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1
Ahire, Shwetal. "Maternal adiposity and plasma concentrations of leptin and adiponectin." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1250701408.
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Ahire, Shwetal V. "Maternal adiposity and the plasma concentration of leptin and adiponectin." Cincinnati, Ohio : University of Cincinnati, 2009. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1250701408.
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Thesis (M.S.)--University of Cincinnati, 2009.<br>Advisor: Debra Krummel. Title from electronic thesis title page (viewed Oct. 20, 2009). Includes abstract. Keywords: pregnancy; skinfold; leptin; adiponectin; obesity. Includes bibliographical references.
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McMath, Arden Lee. "Associations Between Physical Activity Level and Adiponectin/Leptin Ratios in Older Adults." Miami University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=miami1556816283317575.
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Rausch, Jamie Ann. "Secondary Data Analysis Investigating Effects of Marine Omega-3 Fatty Acidson Circulating Levels of Leptin and Adiponectin in Older Adultswith Chronic Venous Leg Ulcers." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu158652907707218.
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Pratap, Anishchal Anshil. "Analysis of adiponectin, leptin and their receptor expression in the 5XFAD mouse model of Alzheimer’s disease." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24135.
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Alzheimer’s disease (AD) is a neurodegenerative disorder that primarily affects individuals over 65 years of age. Pathological hallmarks of the disease include amyloid plaques and neurofibrillary tangles. Individuals with metabolic syndromes such as obesity and type-2 diabetes share similar pathologies with AD patients including insulin resistance, cortical atrophy and neuroinflammation. Adipocyte-derived leptin and adiponectin regulates metabolism, energy expenditure and satiety via their receptors, LepR, AdipoR1 and AdipoR2, respectively. Impaired leptin and adiponectin signalling causes metabolic dysregulation in obesity and diabetes. To determine the role of metabolic dysregulation in the AD brain, this thesis focusses on the expression profiles of leptin and adiponectin receptors and their relationship with neuroinflammation in the brain of the 5XFAD mouse model of AD. Expression of AdipoR1 and AdipoR2 in the brains of 5XFAD mice at advanced stages of the disease was investigated in chapter two. Utilizing immunofluorescent staining, neuronal expression of AdipoR1 and AdipoR2 was significantly reduced and robust expression of AdipoR2 by reactive astrocytes was observed in 5XFAD mice compared to age-matched controls. AdipoR2-expressing astrocytes were also observed in regions regulating metabolism, including the dorsomedial hypothalamic and thalamic paraventricular nuclei in the 5XFAD brain. Increased inflammation surrounding metabolic centres and decreased neuronal AdipoR1 and AdipoR2 suggests metabolic disturbance in 5XFAD mice. Leptin expression in the 5XFAD brain was investigated in chapter three. Analysis utilizing immunofluorescent staining on 5XFAD mice at early and late stages of AD revealed an age-related perturbation of neuronal leptin and LepR expression. Astrocytic expression of leptin and LepR was robust in aged 5XFAD mice and accompanied increased plaque loading and neuroinflammation, compared to younger 5XFAD animals. The shift in LepR, AdipoR1 and AdipoR2 expression from neurons to astrocytes in aged 5XFAD mice suggests that astrocytes may utilize leptin and adiponectin signalling to mediate their reactive state to degrade amyloid in the AD brain. Taken together, these findings provide evidence of impaired leptin and adiponectin signalling in the AD brain.
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Barsnick, Rosa. "Hormones of Energy Metabolism in Critically Ill Foals: Insulin, Glucagon, Leptin, Adiponectin, Ghrelin and Growth Hormone." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1275523617.
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Jacobson, Sofie. "Severe sepsis : epidemiology and sex-related differences in inflammatory markers." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96214.
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Background. Sepsis is a syndrome associated with high mortality rates, substantial morbidity and high costs of care. The incidents of sepsis is reported to be high and controversy exists whether gender affect severity or outcome. Little is known about factors determining susceptibility for developing the syndrome and severity of the syndrome once developed. Early detection and adequate antibiotic administration are the mainstay of treatment and means to identify patients with particular high risk of adverse outcome are desirable. There are data to suggest that the course of sepsis and outcome from the syndrome may be influenced by inherited differences in the immunological response among humans Aims: Paper I: Assess incidence and outcome for ICU-treated sepsis patients in this region; Paper II: Assess if there are gender differences related to characteristics, aspects of treatment or outcome in sepsis in this region. Paper III: Assess the association of baseline levels of leptin and adiponectin and future sepsis event, and association of these adipokines in the cute phase and sepsis severity and outcome. Paper IV: Assess association of baseline levels of mannose-binding lectin (MBL) and future sepsis event, and MBL levels in the acute phase in relation to sepsis severity and outcome. Results. Paper I: Overall ICU mortality rate was 25%, while the ICU mortality for patients with septic shock was 58% in this retrospective single university hospital cohort analysis. Cardiovascular disease and diabetes were the most prevalent comorbidities among patients who died during hospital stay. Paper II: No gender-related differences in mortality or length of stay was found in this prospective single center observational study. Differences in aspects of treatment were related to differences in site of infection. Men had more often infections in skin and skin-structures, whereas women more often had abdominal infections. Early organ dysfunction assessed as SOFA score at admission was a stronger predictor for hospital mortality for women than for men. The discrepancy was related to the SOFA coagulation-sub score. Paper III: In this nested case-referent study hyperleptinemia at baseline predicted a first-ever sepsis event, even after adjustment for BMI and other cardiovascular risk factors. Hyperleptinemia in the acute sepsis phase was associated with reduced risk of in-hospital death in men, but associated with increased risk of in-hospital death in women. Paper IV: In the same matched cohort as in Paper III high baseline levels of MBL predicted a first ever sepsis event. High MBL levels in the acute phase or an increase from baseline to the acute phase associate with increased in-hospital death in women but not in men. Low MBL levels was not identified as a risk for acute sepsis or in-hospital death. Conclusions. Mortality from severe sepsis is high, equally affecting men and women. There are differences in patient characteristics and inflammatory markers, which associate with in-hospital mortality differentially in men and women. Aspects of gender should be mandatory, and genetic analysis are desired in future sepsis research.
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Dinca, Madalina, Maria-Corina Serban, Amirhossein Sahebkar, et al. "Does vitamin D supplementation alter plasma adipokines concentrations? A systematic review and meta-analysis of randomized controlled trials." Elsevier B.V, 2016. http://hdl.handle.net/10757/605887.
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We aimed to elucidate the role of vitamin D supplementation on adipokines through a systematic review and a meta-analysis of randomized placebo-controlled trials (RCTs). The search included PUBMED, Scopus, Web of Science and Google Scholar through July 1st, 2015. Finally we identified 9 RCTs and 484 participants. Meta-analysis of data from 7 studies did not find a significant change in plasma adiponectin concentrations following vitamin D supplementation (mean difference [MD]: 4.45%, 95%CI: -3.04, 11.93, p=0.244; Q=2.18, I(2)=0%). In meta-regression, changes in plasma adiponectin concentrations following vitamin D supplementation were found to be independent of treatment duration (slope: 0.25; 95%CI: -0.69, 1.19; p=0.603) and changes in serum 25-hydroxy vitamin D [25(OH)D] levels (slope: -0.02; 95%CI: -0.15, 0.12; p=0.780). Meta-analysis of data from 6 studies did not find a significant change in plasma leptin concentrations following vitamin D supplementation (MD: -4.51%, 95%CI: -25.13, 16.11, p=0.668; Q=6.41, I(2)=21.97%). Sensitivity analysis showed that this effect size is sensitive to one of the studies; removing it resulted in a significant reduction in plasma leptin levels (MD: -12.81%, 95%CI: -24.33, -1.30, p=0.029). In meta-regression, changes in plasma leptin concentrations following vitamin D supplementation were found to be independent of treatment duration (slope: -1.93; 95%CI: -4.08, 0.23; p=0.080). However, changes in serum 25(OH)D were found to be significantly associated with changes in plasma leptin levels following vitamin D supplementation (slope: 1.05; 95%CI: 0.08, 2.02; p=0.033). In conclusion, current data did not indicate a significant effect of vitamin D supplementation on adiponectin and leptin levels.<br>Revisión por pares
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Nickisch, Sabine. "Glukosetoleranz 24 Stunden postpartal und deren Beziehung zu anthropometrischen Daten sowie Adipozytokinserumkonzentrationen." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-101180.
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Während der Schwangerschaft vollziehen sich im Körper der Frau verschiedene Adaptionsmechanismen, um eine bestmögliche Versorgung für das heranwachsende Kind zu gewährleisten. Bei fortschreitender Gravidität entwickelt sich eine physiologische Insulinresistenz. Gelingt es den maternalen Betazellen des Pankreas‘ nicht, diese zu kompensieren, kann eine diabetische Stoffwechsellage bis hin zur Ausbildung eines Gestationsdiabetes (GDM) entstehen.
Adipozytokine beeinflussen direkt lokale und periphere metabolische, endokrinologische sowie immunologische Prozesse. Inwieweit sie in der Gravidität eine Rolle spielen, ist bislang nicht hinreichend geklärt. In verschiedenen Studien wurde eine Beziehung zwischen den Fettgewebshormonen und der Glukosetoleranz in der Schwangerschaft nachgewiesen. Im Rahmen dieser Dissertation sollte eine Analyse zur Glukosetoleranz und zu Adipozytokinserumspiegeln bei Frauen unmittelbar nach der Entbindung vorgenommen werden. Ergebnisse oraler Glukosetoleranztests von gesunden Frauen 24 Stunden postpartal (n=65) wurden mit denen einer nicht-schwangeren, gesunden Kohorte (n=30) verglichen. Maternale und neonatale anthropometrische Daten wurden in Zusammenhang zu Adipozytokinen gestellt. Im Vergleich zu Frauen mit normaler Glukosetoleranz (NGT) postpartal konnten in dieser Studie signifikant verminderte Blutglukose – sowie nüchtern – Proinsulinspiegel in der nicht-schwangeren Kontrollgruppe nachgewiesen werden, wohingegen die nüchtern-C-Peptidspiegel erhöht waren. Weiterhin zeigten sich postpartal signifikant niedrigere Adiponektin-, aber höhere sOB-R- (soluble leptin receptor) sowie Leptinspiegel der NGT-Mütter im Vergleich zur Kontrollgruppe. Zusätzlich konnte eine Beziehung zwischen Adipozytokinserumspiegeln und Parametern der Glukosetoleranz bzw. Adipositas demonstriert werden. Daraus lässt sich die These ableiten, dass Frauen in der frühen Phase nach der Entbindung ähnliche biochemische Konstellationen wie beim metabolischen Syndrom, der gestörten Glukosetoleranz oder bei Störungen des Adipozytokinsystems aufweisen.
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Will, Katja [Verfasser]. "Untersuchungen zum Einfluss der Adipokine Adiponectin und Leptin auf das Wachstum porciner Skelettmuskelzellen in vitro / Katja Will." Greifswald : Universitätsbibliothek Greifswald, 2014. http://d-nb.info/1053684789/34.
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Thompson, Olivia M. "Risk and protective factors for Barrett's esophagus /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/6605.
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Oliveira, Miriane de [UNESP]. "Diferentes doses de Triiodotironina (T3) aumentam a expressão gênica de leptina, adiponectina e TRα com o envolvimento da via fosfatidil inositol 3 quinase (PI3K) em adipócitos, 3T3-L1". Universidade Estadual Paulista (UNESP), 2016. http://hdl.handle.net/11449/136244.
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Previous issue date: 2016-02-29<br>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)<br>Os hormônios tireoidianos (HT) são essenciais para a sobrevivência, estando envolvidos nos processos de desenvolvimento, crescimento e metabolismo. As ações dos HT são distintas para diferentes órgãos alvos, e podem ocorrer por meio de seus receptores TRα e TRβ, ou por vias alternativas, as quais podem envolver a integrina αvβ3, as proteínas quinases ativadas por mitógenos (MAPK) e a fosfatidil inositol 3 quinase (PI3K). O tecido adiposo (TA) representa um importante alvo dos HT; produzem várias substâncias biologicamente ativas com diferentes funções fisiológicas, denominadas adipocinas, entre elas a leptina e adiponectina. A leptina é considerada um sinal adipostático ao cérebro e está envolvida na regulação do balanço energético. Adiponectina está envolvida em importantes efeitos metabólicos, como estimulação da oxidação de ácidos graxos, redução da gliconeogênese e aumento da termogênese. Vários estudos têm procurado relacionar a síntese de leptina e adiponectina com os HT; entretanto, os resultados obtidos são controversos. O objetivo desse trabalho foi avaliar o envolvimento da via PI3K nos efeitos da triiodotironina (T3) sobre a expressão gênica de leptina, adiponectina e do TRα em cultura de adipócitos, 3T3-L1. Para isso utilizamos inibidor da via PI3K, LY294002 e inibidor da síntese proteica (ciclohexamida - CHX), para verificar se ação do T3 é direta ou indireta. Após a diferenciação das células 3T3-L1 elas foram incubadas por uma hora com T3 na presença ou ausência dos inibidores citados acima. Posteriormente ao período de tratamento foi realizada a análise de expressão gênica de mRNA (leptina, adiponectina e TRα) por RT- PCR e de proteina (leptina) pela técnica de Western Blot. Os resultados para leptina, assim como para TRα, demonstraram a ativação da via de sinalização PI3K para ação do T3 na expressão gênica desses genes, sendo que essa ação pode ser indireta ou direta, dependendo da dose de hormônio administrada. Em relação a adiponectina, a dose suprafisiológica de T3 (sem a ativação da via PI3K) ou desativação da via PI3K eleva os níveis dessa adipocina, e constatamos que a ação do T3, nessa dose, sobre os níveis de mRNA de adiponectina é indireta em adipócitos, 3T3-L1. Em resumo, durante uma hora de tratamento, diferentes doses de T3 aumentam os níveis de expressão das adipocinas, leptina e adiponectina, e do TRα em cultura celular de adipócitos, 3T3-L1, e a via de sinalização PI3K se faz importante para a ação do T3.<br>The thyroid hormones (HT) are essential for survival, being involved in the processes of development, growth and metabolism. Process actions are distinct for different organs, and may occur either directly through its receptors TRα and TRβ, or indirectly through alternative pathways, which may involve integrin αvβ3, the mitogen-activated protein kinases (MAPK) or phosphatidyl inositol 3 kinase (PI3K). Adipose tissue (TA) is an important target of HT; it produces various biologically active substances with different physiological functions, called adipokines, including leptin and adiponectin. Leptin is considered an adipostatic signal to the brain and is involved in the regulation of energy balance. Adiponectin is involved in important metabolic effects, such as stimulating fatty acid oxidation, reducing gluconeogenesis and increasing thermogenesis. Several studies have sought to relate the leptin and adiponectin synthesis with HT, however the results are controversial. The present study aimed to examine the effects of triiodothyronine (T3), on the modulation of leptin, adiponectin and TRα expression and the involvement of the PI3K signaling pathway in adipocytes, 3T3-L1, cell culture. Will be used pathway inhibitors PI3K, LY294002, and protein synthesis inhibitors (cycloheximide - CHX), to examine whether directly or indirectly T3 action. After the differentiation of the cells 3T3-L1 will be incubated by one hour with T3 in the presence or absence of the inhibitors mentioned above. After hormone treatment was measured the of leptin, adiponectin and TRα gene expression using RT-PCR in real time, it was also assessed the expression of leptin by Western blot. The results to leptin, as well as TRα, demonstrated that the activation of the PI3K signaling pathway has a role in TH-mediated direct or indirect gene expression, depending on the dose administered. Regarding adiponectin, T3 supraphysiological dose (without activation of the PI3K pathway) or deactivation of the PI3K pathway raises the levels of this adipokine in adipocytes, 3T3-L1. In summary, during an hour of treatment, different doses of T3 increase of adipokines levels of expression, leptin and adiponectin, and TRα in cell culture of adipocytes 3T3-L1 and PI3K signaling pathway becomes important for action T3.
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Oliveira, Miriane de. "Diferentes doses de Triiodotironina (T3) aumentam a expressão gênica de leptina, adiponectina e TRα com o envolvimento da via fosfatidil inositol 3 quinase (PI3K) em adipócitos, 3T3-L1". Botucatu, 2016. http://hdl.handle.net/11449/136244.
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Orientador: Celia Regina Nogueira<br>Resumo: Os hormônios tireoidianos (HT) são essenciais para a sobrevivência, estando envolvidos nos processos de desenvolvimento, crescimento e metabolismo. As ações dos HT são distintas para diferentes órgãos alvos, e podem ocorrer por meio de seus receptores TRα e TRβ, ou por vias alternativas, as quais podem envolver a integrina αvβ3, as proteínas quinases ativadas por mitógenos (MAPK) e a fosfatidil inositol 3 quinase (PI3K). O tecido adiposo (TA) representa um importante alvo dos HT; produzem várias substâncias biologicamente ativas com diferentes funções fisiológicas, denominadas adipocinas, entre elas a leptina e adiponectina. A leptina é considerada um sinal adipostático ao cérebro e está envolvida na regulação do balanço energético. Adiponectina está envolvida em importantes efeitos metabólicos, como estimulação da oxidação de ácidos graxos, redução da gliconeogênese e aumento da termogênese. Vários estudos têm procurado relacionar a síntese de leptina e adiponectina com os HT; entretanto, os resultados obtidos são controversos. O objetivo desse trabalho foi avaliar o envolvimento da via PI3K nos efeitos da triiodotironina (T3) sobre a expressão gênica de leptina, adiponectina e do TRα em cultura de adipócitos, 3T3-L1. Para isso utilizamos inibidor da via PI3K, LY294002 e inibidor da síntese proteica (ciclohexamida - CHX), para verificar se ação do T3 é direta ou indireta. Após a diferenciação das células 3T3-L1 elas foram incubadas por uma hora com T3 na presença ou ausênci... (Resumo completo, clicar acesso eletrônico abaixo)<br>Abstract: The thyroid hormones (HT) are essential for survival, being involved in the processes of development, growth and metabolism. Process actions are distinct for different organs, and may occur either directly through its receptors TRα and TRβ, or indirectly through alternative pathways, which may involve integrin αvβ3, the mitogen-activated protein kinases (MAPK) or phosphatidyl inositol 3 kinase (PI3K). Adipose tissue (TA) is an important target of HT; it produces various biologically active substances with different physiological functions, called adipokines, including leptin and adiponectin. Leptin is considered an adipostatic signal to the brain and is involved in the regulation of energy balance. Adiponectin is involved in important metabolic effects, such as stimulating fatty acid oxidation, reducing gluconeogenesis and increasing thermogenesis. Several studies have sought to relate the leptin and adiponectin synthesis with HT, however the results are controversial. The present study aimed to examine the effects of triiodothyronine (T3), on the modulation of leptin, adiponectin and TRα expression and the involvement of the PI3K signaling pathway in adipocytes, 3T3-L1, cell culture. Will be used pathway inhibitors PI3K, LY294002, and protein synthesis inhibitors (cycloheximide - CHX), to examine whether directly or indirectly T3 action. After the differentiation of the cells 3T3-L1 will be incubated by one hour with T3 in the presence or absence of the inhibitors mentioned ... (Complete abstract click electronic access below)<br>Doutor
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Khukhlina, O. S. "The contents of cytokeratin 18, adiponectin and leptin in patients with comorbid course of nonalcoholic steatohepatitis and coronary heart desease." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18092.
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Eriksson, Maria. "Adipocyte-derived hormones and cardiovascular disease." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36679.
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Obesity is increasing globally and related to major changes in lifestyle. This increase is associated with an increased risk of cardiovascular disease (CVD). Knowledge about adipose tissue as a metabolic-endocrine organ has increased during the last few decades. Adipose tissue produces a number of proteins with increased body weight, many of which are important for food intake and satiety, insulin sensitivity, and vessel integrity, and aberrations have been related to atherosclerosis. Notably, the risk for developing CVD over the course of a lifetime differs between men and women. In Northern Sweden, men have a higher risk for myocardial infarction (MI). However, the incidence is declining in men but not in women. These sex differences could be due to functional and anatomical differences in the fat mass and its functions. The primary aim of this thesis was to evaluate associations between the adipocyte-derived hormones leptin and adiponectin, and fibrinolysis and other variables associated with the metabolic syndrome, and particularly whether these associations differ between men and women. Another aim was to evaluate these associations during physical exercise and pharmacological intervention (i.e. enalapril). Finally, whether leptin and adiponectin predict a first MI or sudden cardiac death with putative sex differences was also investigated. The first study used a cross-sectional design and included 72 men and women recruited from the WHO MONICA project. We found pronounced sex differences in the associations with fibrinolytic variables. Leptin was associated with fibrinolytic factors in men, whereas insulin resistance was strongly associated with all fibrinolytic factors in women. The second study was an experimental observational study with 20 men exposed to strenuous physical exercise. During exercise, leptin levels decreased and adiponectin levels increased, and both were strongly associated with an improved fibrinolytic capacity measured as decreased PAI-1 activity. Changes in insulin sensitivity were not associated with changing adiponectin levels. The third study was a randomised, double-blind, single centre clinical trial including 46 men and 37 women who had an earlier MI. The study duration was one year, and participating subjects were randomised to either placebo or ACE inhibitor (i.e. enalapril). Circulating leptin levels were not associated with enalapril treatment. During the one-year study, changes in leptin levels were associated with changes in circulating levels of tPA mass, PAI-1 mass, and tPA-PAI complex in men, but not vWF. These associations were found in all men and men on placebo treatment. In women on enalapril treatment there was an association between changes in leptin and changes in vWF. In the fourth study, the impact of leptin, adiponectin, and their ratio on future MI risk or sudden cardiac death was tested in a prospective nested casecontrol study within the framework of the WHO MONICA, Västerbotten Intervention Project (VIP), and Västerbotten Mammary Screening Program (MSP). A total 564 cases (first-ever MI or sudden cardiac death) and 1082 matched controls were selected. High leptin, low adiponectin, and a high leptin/adiponectin ratio independently predicted a first-ever MI, possibly with higher risk in men in regards to leptin. The association was found for non-fatal cases with ST-elevation MI. Subjects with low adiponectin levels had their MI earlier than those with high levels. In conclusion, the adipocyte-derived hormones leptin and adiponectin are related to the development of CVD with a sex difference, and fibrinolytic mechanisms could be possible contributors to CVD risk.
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Majebi, Andrew. "The Role of adipokines in obesity related beta-cell failure of diabetes mellitus and endothelial cell dysfunction of cardiovascular diseases." Thesis, University of Wolverhampton, 2014. http://hdl.handle.net/2436/550229.
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Obesity affects about 520 million people world-wide and more recently studies have shown that fat cells produce proteins called adipokines which have various influences on the human metabolism and has helped to change the perspectives of researchers on the concept of the adipose tissue being just a store of energy. As a result of this, adipokines have been reported to represent a connection between obesity and cardiovascular diseases (CVD) and diabetes mellitus. The concentrations and the bases of the effects of the adipokines in beta cell failure of diabetes mellitus and endothelial cell dysfunction of cardiovascular diseases are still not fully understood. The effect of leptin and adiponectin, which are two adipokines with opposing effects, has been explored in this study. In the present study, therefore, the concentrations of leptin and adiponectin with significant effect on beta cell and endothelial cell function and the basis of these functions were explored. Also, attempts were made in the present study to correlate the concentrations of leptin and adiponectin with possible clinical pointers to complications. In order to achieve this, beta cells (BTC) were grown, made into pseudo-islets (which are said to produce more insulin) and treated with various concentrations of leptin and adiponectin and cells assayed for insulin and amylin (to investigate the role of amylin in insulin secretion). Also the cells were collected and mRNA extracted from these cells, reverse transcription PCR carried out to find out the role of protein phosphatase 1 (PP-1) in the effect of leptin on insulin secretion. PP-1 is a substrate that increases insulin secretion by allowing calcium influx into the cell and is said to be blocked by leptin). Leptin at 500ng/ml was found to significantly (p<0.05) inhibit the secretion of insulin and the expression of PP1 gene, thus supporting this as a basis for the effect of leptin on insulin secretion. Adiponectin however increased insulin secretion significantly but was not as consistent in its effect as leptin was in inhibiting insulin secretion. In order to explore the role of adipokines in cardiovascular diseases, EAHY human endothelial cells were cultured and treated with various concentrations of adiponectin and leptin both individually and in combinations and cells collected and mRNA extracted in order to carry out a reverse transcription PCR for the expression of angiogenic (TIMP2, TIMP3 and MMP2) genes and atherosclerotic (LPA and LPL) genes. Leptin (1nM) was shown to increase the expression of atherosclerotic and angiogenic genes while adiponectin (100nM) inhibited the expression of the atherosclerotic and angiogenic genes. A combination of leptin and adiponectin caused a reduction in the stimulatory effect of leptin on the expression of atherosclerotic and angiogenic genes. This shows that leptin may predispose to CVD while adiponectin reduces the risk of CVD. The clinical part of this study involved recruiting 150 patients with diabetes after the ethical approval for the clinical study was granted. The data collected from the patients included their age, sex, race, and physical parameters like the body mass index (BMI). Also blood samples were collected to measure the clinical indicators for CVD and renal function such as cholesterol, HDL levels, eGFR, albumin levels and their retinopathy status checked as these are the common complications seen in diabetic patients. The blood samples were also assayed in the laboratory for leptin and adiponectin levels and the leptin, adiponectin and the leptin/adiponectin ratio (LAR) were then correlated with the laboratory determinants of CVD, renal and retinopathy risks. It was found that the LAR and the leptin levels correlates significantly with the BMI, while the leptin levels were significantly correlated with the risk of nephropathy in diabetic patients while adiponectin levels correlated significantly with a reduced risk for developing CVD. The role of the enzymes in the leptin and adiponectin signaling pathway was also explored and it was discovered that ERK, P38 and AMPK all had roles in the effect of leptin and adiponectin on the expression of atherosclerotic and angiogenic genes. These data indicate that leptin and adiponectin play significant roles in the beta cell and endothelial cell function and are links between obesity and CVD and diabetes mellitus.
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Castro, Natalia Candido de. "Niveis de leptina e adiponectina em mulheres com falencia ovariana prematura." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308772.
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Orientadores: Cristina Laguna Benetti Pinto, Heraldo Mendes Garmes<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas<br>Made available in DSpace on 2018-08-13T23:30:16Z (GMT). No. of bitstreams: 1
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Previous issue date: 2009<br>Resumo: Mulheres com falência ovariana prematura (FOP) apresentam hipoestrogenismo por falência gonadal antes dos 40 anos de idade, o que se associa a diferentes riscos à saúde, incluindo maior risco para doença cardiovascular (DCV). Não é elucidado o mecanismo de associação entre hipoestrogenismo e leptina e adiponectina, adipocinas que têm sido estudadas, respectivamente, como fator preditor e protetor de DCV. Objetivo: Avaliar os níveis de leptina e adiponectina em mulheres hipoestrogênicas devido à FOP, comparativamente aos de mulheres normoestrogênicas. Sujeitos e Métodos: Estudo tipo coorte transversal realizado no Ambulatório de Ginecologia Endócrina do Departamento de Tocoginecologia da Faculdade de Ciências Médicas, UNICAMP. Foram avaliadas 60 mulheres divididas em dois grupos: 30 mulheres com FOP sem uso de terapia hormonal há pelo menos três meses; e 30 mulheres eumenorreicas, pareadas por idade e índice de massa corpórea (IMC). Foram dosados os níveis de leptina e adiponectina através do método de "Elisa". Os resultados foram descritos como média, desvio padrão e mediana. Os grupos foram comparados utilizando-se testes estatísticos de t de Student e teste de Wilcoxon pareados. Através do coeficiente de Spearman analisou-se a correlação entre a leptina e adiponectina e as mulheres FOP e eumenorreicas, e as variáveis idade, peso e IMC. Resultados: As mulheres com FOP apresentaram idade média de 34,4 ± 5,3 anos e IMC de 24,7 ± 6,3 kg/m2. As mulheres em eumenorréia apresentaram idade média de 34,2 ± 5,6 anos e IMC de 24,5 ± 4,6 kg/m2. Os níveis de adiponectina não diferiram entre os grupos. Os níveis de leptina foram menores entre as com FOP do que no grupo de eumenorreicas (8,8 ± 12,2 e 12,2 ± 9,7ng/ml, respectivamente, p= 0,03). No grupo FOP observou-se uma correlação significativa, porém fraca, entre leptina e peso (r = 0,383, p =0,03). No grupo de mulheres eumenorreicas, a leptina correlacionou-se positivamente com a idade, peso e IMC (r =0,402, p=0,0275; r=0,638, p=0,0006 e r=0,590, p=0,0006, respectivamente). Não houve correlação entre a adiponectina e as variáveis estudadas entre os dois grupos. Conclusão: Os resultados deste estudo apontam para uma influência do estrógeno sobre os níveis de leptina, com redução em condição de hipoestrogenismo, independente da idade e do IMC. A adiponectina não esteve relacionada com o nível estrogênico. Palavras-chave: adipocinas, leptina, adiponectina, menopausa, hipoestrogenismo, falência ovariana prematura<br>Abstract: Women with FOP shows hypoestrogenism due gonadal function loss before the age of 40 years, is associated with a different health risks, included cardiovascular disease (CVD). It isn't not clear the relationship between hypoestrogen and leptin and adiponectin levels, adipokines that has bees studied, respectively, as risk and protection for CVD. Objective: To evaluate serum leptin levels and serum adiponectin levels in premature ovarian failure women (POF). Methods: A cross-sectional study that was carried out at University of Campinas. Sixty participants were divided into two groups. Group 1 was composed of 30 women with premature ovarian failure who hadn't received estrogen-progestin therapy, and group 2 was composed of 30 age-matched and body mass index-matched women with regular menstrual cycles. We measured serum leptin and serum adiponectin levels by "Elisa" methods. The results were expressed as media ± SD and the groups were compared by Student t and Wilcoxon test. Correlation was analyzed by Spearman coefficient between estrogen status and leptin and adiponectin. Results: The media of age in group 1 was 34.4± 5.3 years and in group 2 was 34.2± 5.6 years. The BMI in group 1 was 24.7± 6.3 kg/m2 and in group 2 was 24.5± 4.6 kg/m2. Serum leptin levels (ng/ml) were significantly lower in group 1 in comparison to group 2 (8.8 ± 12.2 e 12.2 ± 9.7 P = 0.03). Serum adiponectin levels (ng/ml) were not significantly different among the two groups. Serum leptin concentration showed a positive, significant correlation with weight (p = 0.03) and had no correlation with age and BMI in the women with POF (group 1). There were no correlation between serum adiponectin level and BMI, weight or age in all studied groups. In the group 2, leptin concentration correlated positively with BMI (r = 0.59, P = 0.0006), weight (r = 0.638, P = 0.0006) and age (r = 0.40, P =0.02). Conclusions: Our results show an influence of estrogen in the leptin levels, with a decreased leptin levels in hypoestrogenism, independently of age and BMI. Adiponectin levels had no correlation with estrogen status<br>Mestrado<br>Tocoginecologia<br>Mestre em Tocoginecologia
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Castro, Natália Pinheiro de. "Relação entre a composição corporal e leptina e adiponectina séricas materna e composição corporal do neonato." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-10102017-133047/.
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A obesidade assim como a gestação está relacionada com distúrbios dos metabolismos da glicose, lipídios, hormônios e produção de moléculas inflamatórias. Portanto, supõe-se que a obesidade na gestação pode influenciar o desenvolvimento do feto, interferindo na sua composição corporal e predispondo a doenças cardiovasculares na idade adulta. Este estudo avaliou a relação entre a composição corporal e leptina e adiponectina séricas materna e a composição corporal de neonatos. A composição corporal de 215 mães e seus respectivos neonatos foi determinada por bioimpedância segmentada e pletismografia por deslocamento de ar, respectivamente. Os níveis séricos de leptina e adiponectina maternos foram avaliados pelo método de Enzyme Linked Immuno Sorbent Assay ELISA. Utilizou-se análise de regressão univariada e análise de regressão linear múltipla para determinar a associação entre fatores maternos e composição corporal do neonato, considerando-se como variáveis resposta a massa de gordura e a massa livre de gordura do neonato. As mães apresentaram idade média de 25,9 (5,2) anos, 43,4 por cento eram pardas e 55,3 por cento pertenciam à classe econômica B. Cerca de 50 por cento das mães apresentaram Índice de Massa Corporal (IMC) pré-gestacional adequado, 27,7 por cento tinham sobrepeso e 10,8 por cento eram obesas.47,1 por cento dos partos foram normal e 29,1 por cento foram cesárea. Nasceram mais crianças do sexo feminino (55,4 por cento) que do masculino e a média de peso ao nascimento foi de aproximadamente 3373 (423) g. O IMC pré-gestacional materno, a massa livre de gordura materna, a massa muscular esquelética materna e a concentração plasmática de adiponectina apresentaram associação positiva com a massa de gordura do neonato. A massa livre de gordura materna, massa muscular esquelética materna e massa muscular do braço direito apresentaram associação positiva com a massa livre de gordura do neonato. A composição corporal materna e a adiponectina, proteína secretada pelo tecido adiposo, exercem influência sobre a composição corporal do neonato. Espera-se que mais estudos sejam conduzidos para investigar os mecanismos envolvidos nos achados desta pesquisa<br>Obesity as well as gestation is related to disturbances of glucose metabolism, lipids, hormones and production of inflammatory molecules. Therefore, it is assumed that obesity during pregnancy can influence the development of the fetus, interfering with its body composition and predisposing to cardiovascular diseases in adulthood. This study evaluated the relationship between body composition and maternal serum leptin and adiponectin and the body composition of neonates. The body composition of 215 mothers and their respective neonates was determined by segmented bioimpedance and air displacement plethysmography, respectively. Serum levels of maternal leptin and adiponectin were assessed by Enzyme Linked Immuno Sorbent Assay ELISA. We used univariate regression analysis and multiple linear regression analysis to determine the association between maternal factors and body composition of the newborn, considering as variables the fat mass and the fat free mass of the newborn. The mothers had a mean age of 25.9 (5.2) years, 43.4 per cent were brown and 55.3 per cent belonged to economic class B. Approximately 50 per cent of the mothers presented Body Mass Index (BMI) adequate pre-gestational age, 27.7 per cent were overweight and 10.8 per cent were obese.47,1 per cent of births were normal and 29.1 per cent were cesarean. More female children (55.4 per cent) were born than male children and the mean birth weight was approximately 3373 (423) g. Maternal pre-gestational BMI, maternal fat-free mass, maternal skeletal muscle mass, and adiponectin plasma concentration were positively associated with neonatal fat mass. The maternal fat free mass, maternal skeletal muscle mass and right arm muscle mass were positively associated with the fat free mass of the newborn. Maternal body composition and adiponectin, a protein secreted by adipose tissue, influence the body composition of the neonate. It is expected that further studies will be conducted to investigate the mechanisms involved in the findings of this research
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Schaarschmidt, Wiebke. "Auswirkungen eines zwölfmonatigen kontrollierten Trainingsprogramms auf die Leptin-, Adiponectin- und Progranulin-Serumkonzentrationen sowie Parameter des Lipidstoffwechsels bei Patienten mit Typ 2 Diabetes." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-78393.
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Die Prävalenz des Typ 2 Diabetes ist in den letzten Jahren deutlich angestiegen. Neben einer gesunden Ernährungsweise ist die Erhöhung der körperlichen Aktivität ein wichtiger Bestandteil in der Basistherapie des Typ 2 Diabetes. Körperliches Training führt zu einer Reihe metabolischer Veränderungen wie zur Reduktion der Fettmasse, zur Verbesserung der Glukosehomöostase, des Lipidprofils und zur Normalisierung zirkulierender Adipokine aus dem Fettgewebe.
Ziel dieser Arbeit war es, die Auswirkungen eines zwölfmonatigen, kontrollierten, praxisnahen, kombinierten Kraft-Ausdauer-Trainingsprogramms auf das Körpergewicht, Parameter des Lipidstoffwechsels (Gesamt-, LDL-, HDL-Cholesterin- und Triglyzerid-Serumkonzentrationen) sowie die Serumkonzentrationen der Adipokine Leptin, Adiponectin und Progranulin bei Patienten mit Typ 2 Diabetes zu untersuchen.
Für die prospektive offene Interventionsstudie wurden initial 710 Patienten mit Typ 2 Diabetes untersucht, von denen 156 die Ein- und Ausschlusskriterien für die Studie erfüllten. Es wurden die Daten von 120 Patienten (77 Frauen, 43 Männer) analysiert, von denen nach Abschluss des zwölfmonatigen Trainingsprogramms vollständige Datensätze vorlagen. Die Patienten trainierten zweimal pro Woche für jeweils 60 + 15 Minuten bei 50-70% ihrer individuellen maximalen Leistungsfähigkeit, die zu Beginn der Studie mittels Spiroergometrie ermittelt wurde. Das Training umfasste jeweils 20 Minuten Aufwärm- und Abkühlphase, 20 Minuten Fahrradergometer-Training, 20 Minuten Training am Rudergerät und 20 Minuten Krafttraining an Krafttrainingsgeräten. Die Messung der Zielparameter erfolgte vor Beginn der Intervention sowie nach drei, sechs und zwölf Monaten körperlichen Trainings.
Das zwölfmonatige Trainingsprogramm führte zu einer signifikanten Reduktion der Gesamt- und LDL-Cholesterin-, Triglyzerid- sowie der Progranulin-Serumkonzentrationen, während sich die zirkulierenden Leptinspiegel nicht veränderten. Die HDL-Cholesterin und Adiponectin-Serumkonzentrationen waren in Folge des Trainingsprogramms signifikant erhöht. Diese Veränderungen waren weitgehend unabhängig von der Entwicklung des Körpergewichts, das sich im Verlauf der Studie nicht signifikant veränderte.
Zusammengefasst zeigt die Untersuchung, dass ein zwölfmonatiges, moderates und praxistaugliches Trainingsprogramm signifikant und unabhängig von Verbesserungen des Körpergewichts die Serumkonzentrationen der Adipokine Adiponectin und Progranulin sowie von Parametern des Lipidstoffwechsels verbessert.
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Mesquita, Carolina Bonfanti. "Associações entre as variações de adipocinas, citocinas inflamatórias e composição corporal em pacientes com doença pulmonar obstrutiva crônica no período de um ano." Universidade Estadual Paulista (UNESP), 2018. http://hdl.handle.net/11449/153450.
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Previous issue date: 2018-02-22<br>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)<br>Introdução: Estudos recentes mostram que o tecido adiposo também contribui para a inflamação sistêmica em pacientes com DPOC. Entretanto, não há dados na literatura que avaliem a variação das adipocinas e suas associações com marcadores inflamatórios, exacerbações e mortalidade em um ano nos pacientes com DPOC. Objetivo: Avaliar as variações das adipocinas, citocinas inflamatórias e composição corporal em pacientes com DPOC no período de um ano. Pacientes e Métodos: Foram avaliados 57 pacientes com DPOC leve a muito grave, destes 6 pacientes morreram, 6 não foram contatados após a avaliação e 5 não quiseram participar da segunda fase estudo, logo realizamos análise de dois momentos dos 40 pacientes que completaram um ano de acompanhamento. No momento basal e após 1 ano foram realizados espirometria pré e pós-broncodilatador, gasometria arterial, exames laboratoriais, oximetria de pulso, dosagem plasmática sérica de interleucina (IL)-6, fator de necrose tumoral alfa (TNF-α), adiponectina e leptina e avaliação sérica laboratorial. Também foi realizado avaliação da composição do corpo, força muscular do quadríceps (FMQ) (MicroFet 2), sensação de dispneia, por meio do Índice de Dispneia Basal (BDI), Escala de Borg e Medical Research Council Modificado (mMRC), avaliação do estado geral de saúde, por meio do questionário de Qualidade de Vida na Doença Respiratória do Hospital Saint George (SGRQ) e Escala Hospitalar de Ansiedade e Depressão (HAD), calculado índice de BODE e Teste de caminhada de 6 minutos. Resultados: Na análise da variação dos 40 pacientes nos dois momentos observamos associação da variação da leptina com a variação de IMC (R:0,43; p=0,006), variação de FMQ E (R:0,42; p=0,008), variação do índice BODE (R:0,39; p=0,024) e variação da IL-6 (R:-0,33; p=0,003). Na análise de regressão linear múltipla apenas observamos associação negativa da variação da IMMC com a variação da adiponectina (coef: -0,35; p=0,03). Não observamos associação das adipocinas na frequência de exacerbação ou mortalidade em um ano. Conclusão: O presente estudo mostrou que a leptina está associada positivamente com a IMC, força muscular periférica e índice BODE e associada negativamente com a IL-6. Novos estudos sobre a variação das adipocinas e suas associações com as variações dos marcadores inflamatórios e do estado nutricional devem ser realizados para melhor esclarecimento.<br>Introduction: Recent studies show that adipose tissue also contributes to systemic inflammation in chronic obstructive pulmonary disease (COPD). However, there are no data in the literature evaluating the evolution of level of adipokines and their associations with systemic inflammation, exacerbations and mortality in COPD patients. Objective: Evaluate the variations of adipokines and their association with systemic inflammation and and body composition in patients with COPD during one year. Patients and Methods: Fifty-seven patients with mild to very severe COPD were evaluated. During the follow up, six patients died, six lost the follow up and five refused to participate in the second assessment. At baseline and after one year we performed post-bronchodilator spirometry, arterial blood gas analysis, laboratory tests, pulse oximetry, serum plasma levels of interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), adiponectin and leptin. We also assessed body composition, peripheral muscle strength (quadriceps), Basal Dyspnea Index (BDI), Borg Scale, and Modified Medical Research Council (mMRC), general health status was evaluated by Saint George Respiratory Questionnaire (SGRQ), Hospital Anxiety and Depression Scale (HAD), BODE index and 6-minute walk test. Results: From the total of 40 patients, we analyzed the variation during one year and we observed a positive association between leptin and BMI (R:0.43; p=0.006), QMS L (R:0.42; p=0.008) and BODE index (R:0.39; p=0.024) and a negative association between IL-6 (R:-0.33; p=0.003). Multiple linear regression showed a negative association between the variation of IMMC and variation of adiponectin levels (coef:-0.35, p=0.03). We did not find association between the frequency of exacerbation and mortality with adipokines. Conclusion: The present study showed that leptin is positively associated with BMI, peripheral muscle strength and BODE index and negatively associated with the IL-6. Further studies on the variation of adipokines and their associations with variations in inflammatory markers and nutritional status should be performed for better clarification.
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Schumacher, Michael Andrew. "Placental Signaling Mechanisms Linking Maternal Obesity, High-Fat Diet, and Adiponectin Levels During Pregnancy to Fetal Overgrowth." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1243013168.
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Mathias, Lucas Solla. "Ativação da via MAPK/ERK e Integrina αvβ3 pela ação da triiodotironina (T3) na modulação da expressão gênica de adipocinas e modificação do perfil lipídico em adipócitos, 3T3-L1". Botucatu, 2019. http://hdl.handle.net/11449/181721.
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Orientador: Miriane de Oliveira<br>Resumo: Introdução: O hormônio triiodotironina (T3) influencia o metabolismo e desenvolvimento do tecido adiposo (TA), modulando a proliferação e diferenciação de adipócitos, podendo agir sobre os reguladores do processo de adipogênese, como o receptor ativado por proliferador de peroxissomo (PPARy). O TA está envolvido na regulação da energia corporal, sintetizando e secretando substâncias denominadas adipocinas, dentre elas a adiponectina e leptina. A adiponectina está relacionada ao aumento da sensibilidade à insulina, enquanto a leptina está envolvida com o gasto energético. O T3 pode desencadear ações por ativação de vias extranucleares, dentre elas a via MAPK/ERK e integrina αVβ3. Objetivo: Verificar a ação do T3, com participação das vias extranucleares MAPK/ERK e integrina αVβ3, na modulação de adiponectina e leptina, além de avaliar os parâmetros relacionados ao perfil adipogênico e dano de DNA. Métodos: Adipócitos, 3T3-L1, foram tratados com T3 (10nM) por uma hora, na ausência ou presença dos inibidores de MAPK/ERK – PD98059 (PD, 50uM) e da integrina αvβ3 – ácido tetraiodotiroácetico (Tetrac, 10-4M). A ausência de qualquer tratamento foi considerada grupo controle (C). Após o período de tratamento foi realizado PCRq-RT para analisar a expressão de mRNA de adiponectina e leptina, e Western Blot para expressão proteica de adiponectina, leptina, PPARy, pAKT e pERK; a viabilidade celular foi realizada pelo ensaio de MTT; a quantificação do acúmulo lipídico pelos ens... (Resumo completo, clicar acesso eletrônico abaixo)<br>Abstract: Introduction: The hormone triiodothyronine (T3) influences the metabolism and development of adipose tissue (TA), modulating the proliferation and differentiation of adipocytes, and can act on regulators of the adipogenic differentiation process, such as the peroxisome proliferator activated receptor). TA is involved in the regulation of body energy, synthesizing and secreting substances called adipokines, among them adiponectin and leptin. Adiponectin is related to increased insulin synaptic, since leptin is involved in energy expenditure. T3 can trigger actions by activation of extranuclear pathways, including MAPK / ERK and integrin α Vβ3. Objective: Given the role of T3 in TA and the importance of adipokines, the objective of this study is to verify the action of T3 with the participation of extranuclear pathways in the modulation of adiponectin and leptin and the parameters related to the adipogenic profile. Methods: Adipocytes, 3T3-L1, were treated with a physiological dose of T3 (10nM) for one hour, in the absence or presence of MAPK / ERK-PD98059 (PD) and integrin αvβ3 - tetraiodothyrocetic (Tetrac) integrin inhibitors. The absence of any treatment was considered as a control group (C). After the treatment period PCRqRT was performed to analyze the expression of leptin and adiponectin mRNA, and Western Blot for protein expression of adiponectin, leptin, PPARγ, pAKT and pERK; cell viability was performed by the MTT assay; the quantification of lipid accumulation by the... (Complete abstract click electronic access below)<br>Mestre
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Rodrigues, Viviane Soares 1985. "Níveis séricos e teciduais de adipocinas, perfil nutricional e papel do tecido mesenterial na doença de Crohn." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311661.
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Orientadores: Raquel Franco Leal, Marciane Milanski Ferreira<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-23T07:39:58Z (GMT). No. of bitstreams: 1
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Previous issue date: 2013<br>Resumo: A doença de Crohn (DC) é caracterizada por uma inflamação de etiologia ainda desconhecida. A hipertrofia do tecido adiposo mesentérico reflete a atividade da doença, uma vez que o mesmo recobre toda a área acometida pela doença. Além disso, os adipócitos sintetizam leptina e adiponectina, adipocinas com ações pró e antiinflamatórias. Objetivo: Avaliar as concentrações séricas de leptina e adiponectina na DC em remissão e em atividade, como também a expressão tecidual de adiponectina na DC em atividade. Casuística e Método: Dezesseis pacientes com DC ileocecal atendidos no ambulatório de Doenças Inflamatórias Intestinais da Universidade Estadual de Campinas participaram do estudo. A análise de leptina e adiponectina foi realizada por ELISA nos pacientes com DC em atividade (grupo DCAT), DC em remissão (grupo DCR) e seis controles saudáveis. Também dez pacientes com DC ileocecal em atividade (grupo DCG) e oito controles (grupo CG) com doença não inflamatória participaram do estudo, para avaliação da adiponectina tecidual. As biópsias foram armazenadas em nitrogênio líquido, e a expressão de adiponectina foi realizada por imunoblot de extrato protéico total. Resultados: Os níveis de proteína C reativa foram maiores no grupo DCAT quando comparado aos demais grupos (p<0,05). Os níveis séricos de adiponectina foram menores no grupo DCAT comparado ao controle, porém não houve diferença entre os grupos DCAT e DCR. A expressão de adiponectina no tecido mesenterial foi significantemente menor no grupo DCG quando comparado ao controle (grupo CG). A leptina sérica foi similar entre os grupos (p>0,05). Os níveis de colesterol total e pré-albumina foram menores no grupo DCAT (p<0,05), quando comparados com o controle. O índice de massa corporal e o nível sérico de triglicérides foram similares entre os grupos. A % de gordura corporal foi menor no grupo DCAT em relação ao controle, e a avaliação subjetiva global mostrou desnutrição no grupo DCAT quando comparado ao DCR. Conclusão: Baixos níveis de adiponectina sérica e mesenterial na DCAT sugerem defeito nos mecanismos antiinflamatórios, o que pode ser responsável pela manutenção do processo inflamatório e hipertrofia da gordura mesenterial próximo à área intestinal afetada, mesmo na presença de baixos níveis de % de gordura corporal<br>Abstract: Crohn's disease (CD) is characterized by inflammation and an etiology that is still unknown. Hypertrophy of mesenteric fat is a reflect of disease activity, since this fat covers the entire length of the affected area. Also, adipocytes synthesize leptin and adiponectin, adipokines responsible for pro and anti-inflammatory effects. Aim: To evaluate serum levels of adiponectin and leptin, as well as mesenterial expression of adiponectin in active CD and those in remission. Casuistic and Methods: Sixteen patients with ileocecal CD followed at the Outpatient Clinic, Coloproctology Unit of University of Campinas Clinical Hospital, participated of the study. Analysis of serum adiponectin and leptin by enzyme linked immunosorbent assay were performed in patients with active CD (DCAT Group), remission CD (DCR Group) and in six healthy controls. Ten patients with active ileocecal CD (DCG Group) and eight patients (CG Group) with non-inflammatory disease selected for surgery were also studied. The specimens were snap-frozen and the expression of adiponectin was determined by immunoblot of protein extracts. Results: Serum C-reactive protein levels were higher in DCAT Group when compared to the others (p<0.05). Serum adiponectin was lower in the DCAT Group when compared to control (p<0.05), but no differences were seen when comparing the DCAT and DCR Groups. Mesenteric adiponectin expression was lower in DCG group when compared to CG group (p<0.05). Serum leptin was similar in all groups (p>0.05). Serum total cholesterol and pre-albumin were lower in the DCAT group when compared to controls (p<0.05). Body Mass Index (BMI) and serum triglycerides were similar among the groups. The percentage of body fat was lower in the DCAT group compared to controls, and the global subjective evaluation showed malnourishing in the DCAT group when compared to DCR group. Conclusion: The lower level of serum and mesenteric adiponectin in active CD suggests a defective regulation of anti-inflammatory pathways, which could be responsible to the maintenance of inflammatory process and hypertrophy of the mesenteric fat tissue nearby the affected intestinal area, even in the presence of low percentage of body fat<br>Mestrado<br>Fisiopatologia Cirúrgica<br>Mestra em Ciências
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Reiner, Christian [Verfasser], Caludia [Akademischer Betreuer] Dellas, Jóse [Akademischer Betreuer] Hinz, and Martin [Akademischer Betreuer] Oppermann. "Die prognostische Bedeutung der Adipozytokine Leptin und Adiponectin bei der akuten Lungenembolie / Christian Reiner. Gutachter: Caludia Dellas ; José Hinz ; Martin Oppermann. Betreuer: Caludia Dellas." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1042733058/34.
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Xie, Linglin Jr. "Understanding adipokine secretion and adipocyte-macrophage cellular interactions, in search for the molecular basis of insulin sensitivity and resistance." Diss., Manhattan, Kan. : Kansas State University, 2008. http://hdl.handle.net/2097/552.
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Colovati, Veronica Luiza Vale Euclydes. "Relação das concentrações de adiponectina, leptina e zinco-α-2-glicoproteína no cordão umbilical com a composição corporal de crianças nos quatro primeiros meses de vida (OU) Relação das concentrações de adiponectina, leptina e zinco-α-2-glicoproteína no cordão umbilical com a composição corporal de lactentes nos 4 primeiros meses de vida." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/89/89131/tde-26052015-141811/.
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A obesidade, caracterizada pelo excesso de tecido adiposo (TA), é uma doença epidêmica com crescente prevalência desde a infância. Os primeiros meses de vida são considerados críticos para o desenvolvimento humano devido a relação com repercussões duradouras na fisiologia do organismo. O TA tem sua formação desde a fase fetal e secreta inúmeras citocinas relacionadas com a obesidade. Destacam-se neste âmbito: a adiponectina, associada à sensibilidade a insulina; a leptina, pela sua interação com o dispêndio energético e a zinco-α-glicoproteína (ZAG) devido à ação moduladora na expansão do TA. Conhecendo-se a importância da ação destas citocinas e a relevância dos primeiros meses de vida sobre a saúde do indivíduo, o objetivo deste estudo do tipo coorte foi analisar as concentrações de adiponectina, leptina e ZAG do cordão umbilical e relacionar com a composição corporal de lactentes do nascimento ao 4º mês de vida. As citocinas foram determinadas no sangue do cordão umbilical por ELISA. A composição corporal foi avaliada mensalmente pelo PEA POD® (Infant Body Composition, Cosmed, USA). Realizou-se análise de variância (ANOVA) para comparações de médias das variáveis qualitativas. A análise de regressão linear múltipla foi utilizada para determinar a relação entre as citocinas e a composição corporal. A adiponectina se associou inversamente com o percentual de gordura no 1º mês de vida em lactentes não alimentadas por leite materno. A leptina mostrou associação positiva com o percentual de massa gorda ao nascimento para o sexo feminino (R²=0,29; P=0.001), porém essa associação não se manteve significante após o primeiro mês de vida. No modelo final estratificado por sexo, a ZAG foi a única variável analisada que explicou o percentual de gordura no 3º mês (R²=0,21; P=0,003) e no 4º mês de vida (R²=0,14; P=0,03) para o sexo feminino. Os resultados desta investigação reforçam a possível influência positiva do papel da leptina no sangue do cordão umbilical no percentual de gordura ao nascimento e do papel da ZAG com influência negativa no percentual de gordura no 3º e 4º meses de vida.<br>Obesity, characterized by excess adipose tissue (AT), is an epidemic disease with increasing prevalence since childhood. The the first months of life are considered critical to human development because of the relationship with long-lasting effects on the physiology of the organism. The TA formation starts in fetal stage and secretes numerous cytokines related to obesity. Stand out in this context: adiponectin is associated with insulin sensitivity; leptin by its interaction with the energy expenditure and zinc-α-glycoprotein due to their modulating effects of the expansion of the TA. Knowing the importance of the action of these cytokines and the relevance of the first months of life on the health of an individual, the aim of this cohort study was to analyze the concentrations of adiponectin, leptin and ZAG cord and relate to body composition of children from birth to 4 months of life. Cytokines were assayed in the cord blood by ELISA. Body composition was assessed by the PEA POD ® (Infant Body Composition, Cosmed, USA) monthly. An analysis of variance (ANOVA) for mean comparisons of qualitative variables. A multiple linear regression analysis was used to determine the relationship between the cytokines and body composition. Adiponectin was inversely associated with the percentage of fat in the 1st month of life in infants not being breast fed. Leptin was positively associated with the percentage of fat mass at birth for females (R ² = 0.29), but this association did not remain after the first month of life. In the final model stratified by sex, ZAG was the only variable that explained analyzed the percentage of fat in 3 (R ² = 0.21) and 4 months (R ² = 0.14) for females. The results of this study reinforce the positive influence of the role of leptin in umbilical cord blood for the percentage of fat at birth and the role of ZAG with negative influence on the percentage of fat in the third and fourth months of life.
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Terrazzan, Ana Carolina. "Níveis de adipocitocinas em sangue de cordão umbilical de recém-nascidos pré- termos de muito baixo peso e recém-nascidos de termo." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/52948.
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Introdução: Adiponectina e leptina são produzidas no ambiente intrauterino, e estão envolvidas no crescimento fetal. Contudo, poucos estudos apresentaram dados de níveis de adiponectina e leptina comparando recém-nascidos (RN) pequenos e adequados para idade gestacional, prematuros de muito baixo peso e a termo. Objetivo: Comparar níveis de adiponectina e leptina em sangue de cordão umbilical de recém-nascidos prematuros muito baixo peso (MBP) e recém-nascidos a termo, e determinar sua relação com peso ao nascer (PN) e ser pequeno (PIG) ou adequado (AIG) para idade gestacional. Métodos: Estudo transversal com recém-nascidos prematuros de muito baixo peso (MBP), com idade gestacional <32 semanas e peso ao nascer <1500g, e recém-nascidos a termo com idade gestacional >37 semanas, nascidos em um hospital terciário, no período de Janeiro de 2010 à Maio de 2011. Critérios de exclusão: presença de malformações congênitas maiores, erros inatos do metabolismo, anomalias cromossômicas. Níveis de adiponectina e leptina em sangue de cordão umbilical foram determinados por enzimoimunoensaio com kit ELISA (R&D Systems). O estudo foi aprovado pelo comitê de ética e pesquisa da instituição sob número (09460). Empregados teste t de Student, Mann-Whitney e regressão linear, e aceito nível de significância p<0.05. Resultados: Ao todo foram estudados 127 recém-nascidos, 55 RNPTMBP e 72 a termo. Gênero, diabetes gestacional, infeção do trato urinário, idade e IMC maternos foram similares em ambos os grupos. Os níveis de adiponectina foram significativamente mais baixo nos recém-nascidos pré-termo do que nos recém-nascidos a termo: 1.57±0.74pg/mL versus 2.4±0.22pg/mL (p<0.001), respectivamente. Os níveis de leptina foram similares entre os grupos: 1.25±0.90pg/mL e 1.38±0.99pg/mL (p=0,481) nos recém-nascidos a termo e prematuros respectivamente. Independente de serem adequados ou pequenos para idade gestacional, RNPTMBP apresentaram níveis de adiponectina mais baixos (p<0,001). Os níveis de leptina e insulina foram similares em ambos os grupos, independentemente de serem AIG ou PIG. Na regressão linear com adiponectina como variável dependente, apenas prematuridade foi estatisticamente significativo. Conclusão: Prematuridade é o principal fator determinante para os baixos níveis de adiponectina em sangue de cordão umbilical em recém-nascidos.<br>Background: Adiponectin and leptin are produced in the intrauterine environment and are involved in fetal growth. However, few studies present data on adiponectin and leptin leves comparing adequate and small for gestational age very low birth weight preterm newborns. Aim: Compare the levels of adiponectin and leptin in cord blood of full term newborns and very low birth weight preterm, and determine its relation with birth weight and being small for gestational age. Methods: Cross sectional study with cord blood adipocytokines dosage in very low birth weight preterm (VLBW), with gestational age (GA) ≤32 weeks and birth weight ≤1500 grams, full term newborns, with GA ≥37 weeks, born at tertiary hospital between January 2010 and May 2011. Exclusion criteria were presence of major congenital malformation, metabolism innate errors, chromosomal anomalies. All includes newborn had a protocol filled with maternal and neonatal data. Adiponectin and leptin levels were determined by ELISA kits (R & D Systems). The study protocol was approved by the institutional review boards and hospital’s ethics committee under the number 09-460. Applied student T test, Mann- Whitney and linear regression. Accepted p <0,05 as significant level. Results: Included 127 newborns, being 55 VLBW preterm and 72 full term. There were no statistic difference regarding gender, maternal gestational diabetes, urinary tract infection, age and BMI. Adiponectin levels were significantly lower in preterm than in full term newborns (1.57±0.74 pg/mL versus 2.4±0.22pg/mL (p<0,001), respectively. Leptin levels were similar in both groups: 1.25 ±0.90pg/mL in full term infants and e 1.38±0.99pg/mL in preterm (p=0,481). When we evaluate adequacy for gestational age inside groups, despite being adequate or small for gestational age, VLBW preterm showed lower levels of adiponectin (p<0,001) and again, there was no statistically significant difference for leptin levels. In the linear regression, prematurity was the only independent variable associated to the low levels of adiponectin (p <0,001). Conclusion: our data suggests that been born prematurely is the main determinant factor for adiponectin levels in umbilical cord of newborns. It’s important to know perinatal factors that may interfere in the secretion of adipocytokines so that it’s possible to develop preventive strategies of metabolic syndrome, not only in adulthood but also in early childhood.
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Sulzbach, Miréia Fortes Vianna. "A interação entre transtorno bipolar e obesidade : avaliação da neuroanatomia hipocampal e de adipocinas séricas." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/131219.
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O Transtorno Bipolar (TB) é uma patologia grave, crônica, associada à alta morbidade e caracterizada por alterações nos estados de humor (mania, hipomania e depressão). Possui comorbidade com diversas patologias clínicas, entre elas a obesidade. Tanto o TB quanto a obesidade possuem um componente imunológico e inflamatório importante. Essa comorbidade é bastante elevada e, quando presente, o paciente tem uma maior probabilidade de possuir déficits na memória declarativa, que está relacionada à disfunção do hipocampo, uma vez que é uma estrutura sensível à inflamação. As adipocinas (por exemplo, a leptina e a adiponectina) são biomarcadores inflamatórios produzidos pelo tecido adiposo que possuem receptores no hipocampo. Assim, o objetivo desta tese é estudar o impacto da obesidade, do tamanho do hipocampo e dos níveis de adipocinas (leptina e adiponectina) em pacientes com TB comparados a controles sem o transtorno. O tamanho do hipocampo foi adquirido com um scanner Philips Achieva de 1,5 Tesla. As dosagens das adipocinas (leptina e adiponectina) foram medidas utilizando kits ELISA-sanduíche. Para ambos os artigos foram selecionados pacientes eutímicos com TB e seus controles. No nosso estudo verificou-se que não há diferença no tamanho do hipocampo total entre pacientes com TB e controles (p = 0,123). Também não há correlação estatisticamente significativa entre o volume do hipocampo total e o IMC na amostra total (p = 0,153, rho = - 0,194), ou nos pacientes com TB (p = 0,084, rho = - 0,345), bem como nos controles (p = 0,823, rho = - 0,043), quando avaliados separadamente. Entretanto, nos pacientes com TB, foi encontrada uma significativa correlação negativa entre os volumes do hipocampo direito e níveis séricos de leptina (r = -0,472, p = 0,021), fato que não se observou entre os controles (r = -0,122, p = 0,563). Nossos resultados sugerem que apesar de não haver sido demonstrada uma associação entre o IMC e o volume do hipocampo, verificou-se que um aumento da leptina sérica nos pacientes com TB está associada com as alterações de volume do hipocampo direito, dados que podem ter tem implicações potencialmente significativas para a nossa compreensão da fisiopatologia do TB. Além disso, embora muito prevalente no TB, a obesidade é um fator de risco modificável, mas negligenciado nos esquemas de neuroprogressão da doença, o que sugere que as intervenções nutricionais são altamente desejáveis para se obter melhores resultados.<br>The Bipolar Disorder (BD) is a serious and chronic illness, associated with high morbidity and characterized by changes in mood states (mania, hypomania and depression). It has several comorbid medical conditions, including obesity. Both BD and obesity have an important immunological and inflammatory component. This comorbidity is quite high and, when present, the patient has an increased likelihood of having deficit in declarative memory, which is related to hippocampal dysfunction since it is a sensitive structure to inflammation. Adipokines (e.g., leptin and adiponectin) inflammatory biomarkers are produced by adipose tissue that have receptors in the hippocampus. The objective of this thesis is to study the impact of obesity, the hippocampus size and levels of adipokines (leptin and adiponectin) in BD patients compared to controls without the disorder. The hippocampus size was acquired with a Philips Achieva 1.5 Tesla scanner. Dosages of adipokines (leptin and adiponectin) were measured using ELISA-sandwich kits. For both articles were selected patients and controls. In our study we found that there was no difference in total hippocampus size between patients and controls (p=0.123). There was no correlation between total hippocampus size and BMI in the whole sample (p=0.153, rho=-0.194), or in BD (p=0.084, rho=-0.345) and controls (p=0.823, rho=-0.043) groups separatedIn patients with BD. However we found a significant negative correlation between the volumes of the right hippocampus and serum leptin levels (p = 0.021, rho = -0.472), a fact that was not observed among controls (p = 0.563, rho = -0.122). Our results suggest that the association between high BMI and increased serum leptin with hippocampal volume changes in patients with BD, has potentially significant implications for our understanding of BD pathophysiology. Furthermore, although very prevalent in BD, obesity is a modifiable risk factor, but neglected in neuroprogressão schemes of the disease, suggesting that the nutritional interventions are highly desirable to obtain best results.
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Ritorto, Vincenzo. "The effect of low birth weight on the expression of PPAR[gamma], adiponectin and leptin in visceral adipose tissue of the 6-month-old lamb /." Title page and abstract only, 2005. http://web4.library.adelaide.edu.au/theses/09SB/09sbr611.pdf.
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Lilja, Mikael. "Trends in obesity and type 2 diabetes : ethnic aspects and links to adipokines." Doctoral thesis, Umeå universitet, Allmänmedicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-49398.
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Objective The prevalence of obesity and related diseases such as type 2 diabetes mellitus (T2DM) is increasing worldwide, and the Asian Indian population seems to be particularly susceptible to developing T2DM, even at a low body mass index (BMI). In Sweden, the age-adjusted prevalence of diabetes has not increased despite increasing self-reported obesity. However, modern data on the prevalence of obesity and T2DM in Scandinavia are absent.The biochemical links between obesity and subsequent T2DM are unknown, but the adipocyte-derived hormones leptin and adiponectin (adipokines) have been suggested as potential links because they both are related to insulin and glucose physiology. Some studies have found leptin to be an independent predictor of T2DM in men but not in women, although these results are inconsistent. In contrast, adiponectin has more consistently been linked to development of T2DM in both men and women. Furthermore, the leptin–adiponectin ratio may predict incident T2DM better than either of the two hormones separately.The aims of this thesis were to describe time trends in obesity and T2DM in northern Sweden, to evaluate leptin and adiponectin as predictors of deterioration in glucose metabolism including T2DM, and to evaluate leptin as a risk marker regarding ethnic differences, circ-annual variation, and intra-individual stability. Materials and methods Three large population surveys were used, the Northern Sweden MONICA (MONitoring of Trends and Determinants in CArdiovascular Disease) study, the Västerbotten Intervention Programme (VIP), and the Mauritius Non-Communicable Disease Study. Within the MONICA study, six cross-sectional surveys were performed in Sweden’s two northernmost counties, Norrbotten and Västerbotten, between 1986 and 2009. A total of 1000 men and 1000 women ages 25–64 years, also including from 1994 250 men and 250 women ages 65–74 years, were independently chosen for each survey. The overall participation rate was 75%. In 1999, a reinvestigation was performed in 74% of all participants from the three first surveys. Data from the MONICA surveys were used in papers I and IV and data from the reinvestigation survey in paper II. VIP is an ongoing population intervention program that started in the mid-eighties targeting cardiovascular risk factors and has covered the whole county of Västerbotten since 1991. Inhabitants are invited the years they turn 40, 50, and 60 years old, and the annual participation rate has varied between 48% and 67%. A subset (n=1780) from VIP was used in paper II for the circ-annual leptin analysis, and VIP data linked to the diabetes register in Västerbotten (DiabNorr) were used in a case referent study (640 patients with T2DM) in paper III. The Mauritius Non-Communicable Disease Study was performed in 1987 in 10 randomly selected (with probability proportional to size) population clusters. All eligible adults ages 25–74 years were invited, and the participation rate was 86% (n=5083). In 1992, a follow-up survey was performed in 49% of the initial participants. The Mauritius survey data were used in paper II. Results I. BMI increased in men ages 25–74 years and in women ages 25–44 years in northern Sweden between 1986 and 2004. The prevalence of obesity (BMI 30) increased in men ages 25–44 and 55–74 years and in women ages 25–44 years. The prevalence of obesity increased from 10.4% to 19.1% in men and from 12.9% to 17.9% in women ages 25–64 years. Waist circumference (WC) decreased in women of all ages and in men ages 55–64 years between 1986 and 1990. After 1990, WC increased again, and the prevalence of abdominal obesity rose markedly in women ages 25–64 years. II. Differences in circulating levels of leptin, leptin per BMI unit (leptin/BMI), and leptin per cm in WC (leptin/waist) were tested in men and women of Asian Indian, Creole (African), and Caucasian ethnicity. Asian Indian men and women had the highest leptin concentrations and Caucasian men and women the lowest while Creole men and women had intermediate values for leptin, leptin/BMI, and leptin/waist. No circ-annual variation in leptin concentrations was seen in Caucasians. The intra-individual test– retest stability for leptin was equal in men and women of different ethnicities, over 5–13 years, with an intra-class correlation of 0.65–0.82. III. High adiponectin concentrations predicted decreased risk of T2DM in both insulin-sensitive and insulin-resistant men and women, whereas high leptin levels predicted increased risk for T2DM only in insulinsensitive men. A high leptin–adiponectin ratio predicted T2DM in both men and women, and men with a high ratio had a shorter time to diagnosis than those with a low ratio. IV. In northern Sweden, fasting and post-load glucose increased in women ages 24–65 years with 0.2 mmol/l and 0.7 mmol/l, respectively, between 1990 and 2009. Consequently, the prevalence of impaired fasting glucose and impaired glucose tolerance (IGT) rose from 4.5% to 7.7%, and from 7.8% to 14.5%, respectively. In men, post-load glucose increased at 0.5 mmol/l, and the prevalence of IGT rose from 3.5% to 10.1%. The prevalence of diabetes did not increase. An independent relationship between leptin and changes in fasting and post-load glucose was seen in men but not in women. Conclusion An increasing obesity and concomitant deterioration in glucose metabolism was seen in northern Sweden in the period studied. High adiponectin concentrations predicted a decreased risk of T2DM in both men and women, whereas high leptin concentrations predicted an increase in fasting and post-load glucose as well as an increased risk of T2DM in men but not in women. Individual insulin resistance status modified the association between leptin and T2DM, and the leptin–adiponectin ratio may add further predictive information beyond the measures of the separate hormones. In relation to traditional anthropometric measures of obesity, Asian Indian men and women had the highest and Caucasians the lowest concentrations of leptin while Creole (African) men and women had intermediate levels. As a risk marker, leptin has a high intra-individual stability, equal in men and women and among different ethnicities over 5–13 years with no circ-annual variation.
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Verde, Sara Maria Moreira Lima. "Papel da adiposidade sobre a concentração de biomarcadores de oxidação e adipocitocinas na neoplasia maligna da mama." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-14122015-145005/.
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Introdução: A neoplasia maligna da mama é a mais frequentes entre as mulheres, respondendo, no Brasil, por 26,3 por cento de todos os cânceres no sexo feminino e por 14 por cento dos óbitos. Sabe-se que a obesidade é também uma doença crônica, que apresenta um panorama epidemiológico crescente, capaz de modificar as concentrações de hormônios esteroides, hormônios do crescimento, que envolve processos inflamatórios crônicos e de baixa intensidade os quais favorecem a proliferação celular e redução da apoptose. Portanto, é plausível que mulheres com câncer de mama que tenham excesso de peso e adiposidade apresentem maior risco para um prognóstico clínico menos favorável. Objetivo: Avaliar o papel da adiposidade sobre a oxidação e as adipocitocinas na neoplasia mamária. Material e Métodos: Estudo observacional do tipo caso-controle, com 101 mulheres com tumor de mama (Caso) e 100 mulheres sem câncer (Controle), selecionadas no Hospital Geral de Fortaleza (Fortaleza-CE), nos anos de 2011 e 2012. Realizou-se avaliações socioeconômicas, clínica (estado de menopausa, uso de terapia de reposição hormonal-TRH, história reprodutiva, amamentação, tabagismo, sedentarismo e história familiar de câncer; estadiamento clínico (EC), tamanho do tumor e presença de linfonodos comprometidos), antropométrica (peso, índice de massa corporal -IMC, circunferência da cintura - CC) e de composição corporal ( por cento Massa Gorda - por cento MG; por cento Massa Magra - por cento MM; Ângulo de fase - AF) por impedância bioelétrica. Após jejum de 12h obteve-se alíquotas de sangue e a partir do plasma analisou-se marcadores de estresse oxidativo [TBARS; LDL(-); anti-LDL(-); 8-OHdG; vitaminas antioxidantes] e adipocitocinas (leptina e adiponectina). Comparação entre os grupos Caso e Controle total e segundo excesso de peso e obesidade foram realizadas por meio dos testes t-Student e Man-Whitney. Modelos de regressão linear simples e múltipla, assim como analises logísticas foram testadas entre variáveis brutas e ajustadas visando identificar associações entre adiposidade e marcadores bioquímicos de estresse oxidativo e adipocitocinas. Todos os testes estatísticos foram realizados no programa estatístico SPSS versão 20.0, onde considerou-se p < 0,05, como nível de significância. Resultados: Os grupos Caso e Controle se mostraram semelhantes em relação aos aspectos socioeconômicos e clínicos. Entre as variáveis antropométricas e de composição corporal apenas a CC (p=0,002) foi maior nas mulheres com tumor de mama. Com relação aos marcadores oxidativos e adipocitocinas, independente da adiposidade e do excesso de peso, o grupo Caso apresentou perfil menos favorável com maiores concentrações plasmáticas de TBARS (p<0,001), LDL(-) (p=0,026), auto-anticorpo anti-LDL(-) (p<0,001) e 8OHdG (p=0,021) e adiponectina (p<0,001) em menores concentrações. Entre as pacientes com tumor de mama, as com excesso de peso mostraram menores concentrações de adiponectina (p=0,018) e maiores de 8OHdG (p=0,02) e leptina (p=0,01), sendo essa adipocitocina 9 associada de modo positivo com CC (p=0,012) e por cento MG (p=0,001). Os nutrientes antioxidantes não se alteraram em função da presença do tumor e tão pouco pelo peso e adiposidade. Entretanto no câncer de mama, retinol e ß-caroteno, estiveram inversamente associados com linfonodos comprometidos (p=0,034) e EC III e IV (p=0,014), respectivamente. O risco de câncer de mama foi maior nos maiores tercis de CC, (OR=2,69; IC=1,33-5,47) TBARS (OR=6,99; IC=2,99-16,32) e Anti-LDL(-) (OR=10,28; IC=4,11-25,75) e nos menores tercis de adiponectina (OR=0,44; IC=0,22-0,91). Conclusão: A adiposidade intensificou as alterações oxidativas e de adipocitocinas promovidas pela neoplasia da mama. A obesidade abdominal aumentou o risco de câncer de mama, bem como as maiores concentrações plasmáticas de marcadores oxidativos, sugerindo prognóstico menos favorável.<br>Introduction: Breast malignant neoplasm is more frequent among women. In Brazil, it corresponds to 26, 3 per cent of all cancers in the female gender and to 14 per cent of the causes of death. It is well known that obesity is also a chronic disease, which presents an increasing epidemiological panorama, capable of modifying the concentrations of steroids hormones, the growth hormones, which involves chronic and low-intensity inflammatory processes, enabling cellular proliferation and the reduction of apoptosis. Therefore, it is plausible that women with breast cancer who are overweight and have adiposity present a higher risk of a less favorable clinical prognosis. Objective: To evaluate the role of adiposity over oxidation and the adipokines on breast neoplasia. Material and Methods: It was an observational study of the case-control type, with 101 women with a breast tumor (Case) and 100 women without cancer (Control), selected at Hospital Geral de Fortaleza (Fortaleza-CE), in the years of 2011 and 2012. Socio-economic evaluations were accomplished, clinic (menopause, use of Hormone Replacement Therapy (HRT), reproductive history, breastfeeding, smoking, sedentarism and family-history of cancer; clinic staging (CS), size of the tumor and presence of affected lymph nodes), anthropometrics (weight, body mass index BMI, waist circumference - WC) and of body composition ( per cent Fat Mass - per cent FM; per cent Lean Mass - per cent LM; Phase Angle - PA) by bioelectrical impedance. After a 12-hour-fasting, blood aliquots were obtained and markers of oxidative stress were analyzed from the plasma [TBARS; LDL(-); ANTI-LDL (-); 8-OHdG, antioxidant vitamins] and adipokines (leptin and adiponectin). The comparison between the groups Case and total Control and according to overweight and obesity were accomplished through the tests t-Student and Man-Whitney. Models of simple and multiple linear regression, as well as logistical analyses were tested among gross and adjusted variables aiming at identifying association between adiposity and biochemical markers of oxidative stress and adipokines. All the statistic tests were accomplished on the statistic program SPSS version 20.0, in which p<0,05 was considered as a level of significance. Results: The groups Case and Control were similar with relation to the socioeconomic and clinic aspects. Among the anthropometric and body composition variables, only CC (p=0,002) was higher in women with breast tumor. With relation to oxidative markers and adipokines, independently from adiposity and overweight, the Case group presented a less favorable profile, with higher plasmatic concentrations of TBARS (p<0,001), LDL (-) (p=0,026), auto-antibody, anti-LDL(-) (p<0,001) and 8OHdG (p=0,021) and adiponectin (p<0,001) in lower concentrations. Among the patients with breast tumor, the overweight ones showed lower concentrations of adiponectin (p=0,018) and higher of 8OHdG (p=0,02) and leptin (p=0,01). This adipokine was associated in a positive way to CC (p=0,012) and FM (p=0,001). The antioxidant nutrients did not alter due to the presence of the tumor or due to weight and 11 adiposity. However, in breast cancer, retinol and beta carotene were inversely associated to affected lymph nodes (p=0,034) and CS III and IV (p=0,014), respectively. The risk of breast cancer was higher in the bigger WC tertiles, (OR=2,69; IC=1,33-5,47) TBARS (OR=6,99; IC=2,99-16,32) and Anti-LDL(-) (OR=10,28; IC=4,11-25,75) and in the smaller adiponectin tertiles (OR=0,44; IC=0,22-0,91). Conclusion: Adiposity intensified oxidative and adipokines alterations promoted by breast neoplasia. Abdominal obesity increased the risk of breast cancer, as well as higher plasmatic concentrations of oxidative markers, suggesting a less favorable prognosis.
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Sete, Manuela Rubim Camara. "Níveis séricos de adipocinas e ácidos graxos em pacientes comperiodontite crônica generalizada." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6653.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior<br>O tecido adiposo é um grande reservatório de mediadores biologicamente ativos, tais como as adipocinas.As principaissãoa leptina, a resistina e a adiponectina,que estão presentes em processos inflamatórios e podem estar diretamente ligadas à doença periodontal. Os ácidos graxos teriam um papel regulador sobre essas adipocinas. O objetivo do trabalho foicomparar as concentrações de leptina, resistina e adiponectina e de ácido docosahexaenoico (DHA), ácido docosapentaenoico(DPA), ácido eicosapentaenoico(EPA) e ácido araquidônico (AA),no sangue dos pacientes com periodontite crônica generalizada e com gengivite. Como objetivo secundário, avaliar a razão entreessas substâncias no soro desses pacientes.Participaram do estudo 15 pacientes sistemicamente saudáveis com periodontite crônica generalizada (grupo teste, idade média: 45.7 9.4 anos) e 15 com gengivite (grupo controle, idade média 32.1 7.8 anos). Foram registrados os parâmetros médicos e periodontais e amostras sanguíneas foram coletadas. As concentraçõesno soro de ácidos graxos foram analisadas por cromatografia gasosa e as adipocinas foram analisadas pelo método multiensaio multiplex. Ascomparações entre as variáveis foram analisadas pelo teste Mann-Whitneye as correlações pelo teste de Spearman. Não houve diferença significante entre os níveis de adipocinas entre os grupos. Quanto aos níveis de DHA, DPA, EPA e AA, houve diferença significativamente maior para o grupo de pacientes com periodontite comparado ao grupo com gengivite.As razões entre res/DHA, res/AA, adipon/DHA, adipon/AA e adipon/DPA foram significantemente menores para o grupo periodontite. Não houve correlação entre as adipocinas e os parâmetros clínicos analisados e entre os níveis de adipocinas e ácidos graxos. Concluímos que aperiodontite crônica generalizada apresenta diferenças significativamente maiores nos níveis dos ácidos graxos quando comparada à gengivite.As adipocinas, resistina e adiponectina,apresentaram uma tendência a valores menores no grupo periodontite. Os resultados das razões sugerem uma menor proporção de resistina e adiponectina em relação aos ácidos graxos na periodontite.<br>Adipose tissue is a large reservoir of biologically active mediators, such as adipokines. The main ones are leptin, resistin and adiponectin, which are present in inflammatory processes and can be directly linked to periodontal disease. Fatty acids might have a regulatory role on these adipokines. The aim of this study was to compare the concentrations of leptin, resistin and adiponectin and docosahexaenoic acid(DHA), docosapentaenoic acid (DPA), eicosapentaenoic acid(EPA) and arachidonic acid (AA), in the blood of patients with generalized chronic periodontitis and gingivitis. Secondary objective was to evaluate the ratio of these substances in the serum of these patients. Participants were 15 systemically healthy patients with chronic periodontitis (test group, mean age: 45.7 9.4 years) and 15 with gingivitis (control group, mean age 32.1 7.8 years). We recorded medical and periodontal parameters and collected blood samples. Serum concentrations of fatty acids were analyzed by gas chromatography and adipokines were analyzed by multiplex bead immunoassay. Comparisons between variables were analyzed by Mann - Whitney test and correlations using the Spearman test. There was no significant difference between the levels of adipokines between groups. Considering the levels of DHA, DPA, EPA and AA, there was difference significantly higher for the group of patients with periodontitis compared to the group with gingivitis. The ratios res/DHA, res/AA, adipon/DHA, adipon/AA and adipon/DPA were significantly lower for the group periodontitis. There was no correlation between adipokines and clinical parameters analyzed and between levels of adipokines and fatty acids. We conclude that generalized chronic periodontitis differs significantly higher levels of fatty acids when compared to gingivitis. Adipokines, resistin and adiponectin, showed a tendency to lower values in periodontitis. Reasonss results suggest a smaller proportion of adiponectin and resistin in relation to the fatty acids in periodontitis.
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Doneda, Divair. "Avaliação do estado nutricional e de parâmetros da homeostase de energia em pacientes com Doença de Gaucher." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/71632.
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INTRODUÇÃO: A doença de Gaucher (DG) é um erro inato do metabolismo causado pela atividade deficiente da enzima glicocerebrosidase e subdivide-se em três tipos: tipo I (DG tipo I), que é o mais frequente e não apresenta comprometimento do sistema nervoso central; o II (DG tipo II), agudo e neuronopático; e o III (DG tipo III), subagudo e neuropático. Todos os tipos caracterizam-se pela heterogeneidade clínica, com manifestações de intensidade distintas, tais como: hepatoesplenomegalia, alterações hematológicas e dores ósseas. Alterações no metabolismo energético também são descritas. A terapia de escolha para a DG é a reposição enzimática (TRE). OBJETIVO PRINCIPAL: Avaliar o estado nutricional e a homeostase de energia em pacientes com DG em TRE. MÉTODOS: A presente tese contemplou 4 etapas: Etapa 1) Elaboração de revisão sistemática da literatura sobre aspectos nutricionais da DG tipo I. Etapa 2) Avaliação da coorte de pacientes acompanhados no Centro de Referência para DG do Rio Grande do Sul (CRDG/RS; n= 38; DG tipo I=35; DG tipo III= 3) quanto a dados relativos ao estado nutricional. Etapa 3) Avaliação do gasto energético basal por calorimetria indireta dos pacientes com DG tipo III do CRDG/RS. Etapa 4) Avaliação, por meio de estudo transversal controlado, dos níveis de grelina, leptina e adiponectina de pacientes com DG tipo I do CRDG/RS, com idade superior a 18 anos e em TRE há mais de 6 meses (n=15); os pacientes foram pareado por sexo, idade e IMC com controles hígidos. RESULTADOS: Etapa 1) Foram localizados 175 estudos, dos quais 28 preencheram os critérios de inclusão. Etapa 2) Avaliação da coorte de pacientes acompanhados no Centro de Referência para DG do Rio Grande do Sul (CRDG/RS; n= 38; DG tipo I=35; DG tipo III= 3) quanto a dados relativos ao estado nutricional. Etapa 2) Os dados antropométricos dos pacientes adultos com DG tipo I (n=31) revelaram que quatorze apresentavam sobrepeso ou obesidade grau I e todos os pacientes com idade inferior a 18 anos estavam com peso e estatura adequados. A idade dos pacientes apresentou alta correlação com o IMC e com o nível de ferritina. O IMC apresentou correlação com a ferritina e esta com o colesterol total e com o LDL-colesterol. O colesterol total apresentou correlação com o HDL, com o LDL e uma correlação negativa com a quitotriosidase. O subgrupo que iniciou o tratamento com idade superior a 18 anos (n=16) teve um aumento significativo de IMC após a TRE (p=0,001) e o que iniciou o tratamento antes de 16 anos (n=10) teve um aumento significativo no escore-z para estatura e IMC (p=0,004 e p= 0,032, respectivamente). Etapa 3) Os pacientes com DG tipo III apresentaram hipermetabolismo e dois deles estavam desnutridos. Etapa 4) A mediana dos níveis de grelina, leptina e adiponectina dos pacientes não diferiu da dos controles. Os níveis de grelina e adiponectina apresentaram correlação positiva entre si e com o HDL-colesterol; e inversa com o IMC, circunferência de cintura e triglicerídeos. Os níveis de leptina apresentaram correlação inversa com o LDL-colesterol e direta com o IMC, circunferência da cintura, dose de enzima, triglicerídeos, insulina e HOMA-IR. Oito pacientes preenchiam os critérios para síndrome metabólica, quatro dos quais estavam com resistência à insulina pelo índice HOMA-IR. CONCLUSÕES: Os dados da revisão sistemática indicaram que o tratamento com imiglucerase melhora os índices de crescimento de crianças e adolescentes com DG tipo I o que está em consonância com os dados encontrados nesta coorte. Em relação aos pacientes avaliados, o estado nutricional classificado pelo IMC mostrou que quase metade dos pacientes com DG tipo I estava com excesso de peso e que a TRE parece contribuir para esse achado. O hipermetabolismo em pacientes com DG tipo III parece constituir-se num biomarcador da gravidade da doença. A leptina apresentou alta associação com a insulina e com o índice HOMA-IR, podendo tornar-se um biomarcador para avaliar indícios precoces de resistência à insulina em pacientes com DG. Aumento de peso, síndrome metabólica e resistência à insulina parecem ser frequentes em pacientes com DG tipo I. Estudos adicionais são necessários para investigar as associações encontradas.<br>INTRODUCTION: Gaucher disease (GD) is an inborn error of metabolism, caused by the deficient activity of the glucocerebrosidase enzyme and is divided into three types: type I, which is the most frequent and does not present neurological compromise; type II, which is acute and neuronopathic; and type III, which is subacute and neuronopathic. All types are characterized by clinical heterogeneity and symptomatic manifestations of varied intensity, such as hepatosplenomegaly, hematologic dysfunction, bone pain; energy homeostasis dysfunction is also present. The choice therapy for GD is enzyme replacement therapy (ERT). OBJECTIVE.To assess the nutritional status and the energy homeostasis in patients affected by Gaucher Disease under enzyme replacement therapy. METHODS.This present study is composed of 4 stages. Stage 1) Systematic literature review on GD type I nutritional aspects. Stage 2) Assessment of data revolving around nutritional status of the patients cohort followed at the GD Reference Center in Rio Grande do Sul(CRDG/RS; n= 38; GD type I=35; GD type III= 3. Stage 3) Assessment of basal energetic expenditure by indirect calorimetry in GD type III patients at CRDG/RS. Stage 4) Assessment, by means of controlled transversal study, of ghrelin, leptin and adiponectin levels in GD- I patients, age over 18 yo and under ERT for at least 6 months (n=15); the patients were pair matched with healthy controls for sex, age and BMI. RESULTS: Stage 1) 175 studies were found, of which 28 met the inclusion criteria. These studies have shown ERT is associated to: growth normalization in children and teenagers with delayed development; partial correction of hypermetabolism and glycemic profile dysfunctions; and increase in weight as well as insulin resistance and development of Diabetes mellitus type 2 in adults. Stage 2) The anthropometric data of adult patients with GD type I (n=31) pointed out fourteen showed overweight or obesity level 1, and all patients aged under 18yo showed adequate weight and height. The patient’s age showed high correlation with BMI and ferritin levels. BMI presented correlation with ferritin and the latter with total cholesterol and LDL- cholesterol. Total cholesterol showed correlation with HDL, with LDL and negative correlation with chitotriosidase. The subgroup comprising those who were over 18 years of age (n=16) at the beginning of treatment had a significant increase in BMI after ERT (p=0,001) and those beginning treatment under the age of 16 showed (n=10) significant increase in the z-score for height and BMI (p=0,004 and p= 0,032, respectively). Stage 3) GD type III patients showed hypermetabolism and two of them (2/3) were malnourished. Stage 4) The median of ghrelin, leptin and adiponectin levels of patients did not differ from that of the controls. The ghrelin and adiponectin levels presented positive correlation between themselves, with HDL-cholesterol, and inverse correlation with BMI, waist circumference, and triglycerides. The leptin levels presented inverse correlation with LDL-cholesterol and direct correlation with BMI, waist circumference, enzyme dose, triglycerides, insulin, and HOMA-IR. Eight patients (n=15) met the criteria for metabolic syndrome, four of which had insulin resistance, as measured by the HOMA-IR index. DISCUSSION AND CONCLUSIONS: Data from the systematic review showed the treatment with imiglucerase improves growth in children and adolescents with GD type I, this meets the findings in this cohort. In relation to the patients assessed, the nutritional status measured by BMI showed that almost half of the GD type I patients were overweight and that ERT seems to contribute to this finding. Hypermetabolism in GD type III patients seems to be a biomarker of the severity of this disease. Leptin presented high association with insulin and with the HOMA-IR index, and may eventually become a biomarker to evaluate early evidence of insulin resistance in GD patients. Weight increase, metabolic syndrome and insulin resistance seem to be frequent in GD type I patients. Further research is necessary to investigate the findings herein researched.
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Salvator, Helene. "Rôle des adipokines dans la régulation de l’activation des macrophages pulmonaires humains." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLV082/document.
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L’obésité est responsable de diverses complications médicales, notamment respiratoires. Elle favorise l’apparition de maladies bronchiques chroniques (asthme, BPCO) et complique leur prise en charge. Elle s’accompagne de troubles respiratoires du sommeil et augmente la susceptibilité aux infections respiratoires.Le tissu adipocytaire est désormais reconnu comme un tissu hormonal, source de nombreux médiateurs dont font partie les adipokines, cytokines produites principalement par les adipocytes. Parmi celles-ci, l’adiponectine (APN) est une protéine de 30kDa qui peut s’associer en multimères de plus ou moins haut poids moléculaire. Ses taux circulants sont élevés mais sa concentration sérique diminue avec le gain de poids.L’adiponectine est impliquée dans les phénomènes d’immunorégulation associés aux modifications nutritionnelles et également dans le développement pulmonaire. Mais le rôle pro ou anti-inflammatoire de l’APN est toujours un sujet à débat. L’association entre les taux sériques d’APN et la survenue de maladies bronchiques n’est pas clairement démontrée chez l’homme.Nous nous sommes intéressés au rôle que joue l’APN au sein du système respiratoire, dans la régulation du fonctionnement des macrophages et cellules épithéliales bronchiques. Nous avons plus particulièrement étudié l’effet de l’APN sur la sécrétion de cytokines par ces deux types cellulaires.Nous disposons de pièces opératoires pulmonaires de patients opérés pour un cancer bronchique, à partir desquelles nous réalisons des cultures primaires d’explants de parenchyme, de macrophages pulmonaires ou de cellules épithéliales bronchiques et nous disséquons des anneaux bronchiques.Nous avons montré qu’il existait une production d’APN in situ par du tissu pulmonaire humain et que cette production était corrélée, à l’instar de la forme circulante, au poids du patient. Nous avons vérifié que les récepteurs à l’APN (AdipoR1 et AdipR2) étaient tous les deux exprimés par des macrophages pulmonaires, des explants de bronches et des cellules épithéliales bronchiques.Nous avons soumis les macrophages pulmonaires humains à un traitement par de l’APN à différentes concentrations (3-10-30 microg/ml) avant de les stimuler par du LPS (10 ng/ml ou Poly I:C 10 ng/ml) ou d’IL-4 (10 ng/ml). Nous avons montré que l’adiponectine diminuait la sécrétion des cytokines M1 induites par le LPS et le Poly I:C (IL6, CCL3, CCL4, CCL5, CXCL8, TNF). tout comme celles des cytokines M2 induites par l’IL-4 (CCL13, CCL18, CCL22). L'adipoRon, agoniste synthétique des récepteurs de l'adiponectine, a montré les mêmes effets que la protéine recombinante.Nous avons comparé avec l’effet d’autres adipokines : la leptine à sa plus grande concentration (1000 ng/ml) induisait la production de cytokines de type M1 (IL6, CCL3, CCL4, CCL5, TNFa) par des macrophages non stimulés alors que la visfatine et la chémérine n’avaient aucun effet sur la production de cytokines par les macrophages.Seule l’adiponectine a démontré un effet sur les cellules épithéliales bronchiques, en modulant de façon opposée la production de certaines cytokines : diminution de la sécrétion de CXCL1 et CCL2 en situation basale et après traitement par TNF (50 ng/ml) mais augmentation de celle d’IL6 et CXCL8 en situation basale.Nous avons complété ce travail par des expériences sur la régulation du tonus bronchique par les adipokines, en utilisant des anneaux bronchiques dans des cuves à organes isolées. Ces résultats ont fait l'objet d’un dépôt de brevet européen.Ces travaux sont les premiers à s’intéresser à l’effet de l’APN et de l’AdipoRon sur un modèle de culture primaire de macrophages et cellules épithéliales bronchiques humains. L’APN est capable de moduler la polarisation de ces cellules. Les adipokines régulent aussile tonus bronchique. Les adipokines sont essentielles à la compréhension du retentissement pulmonaire de l’obésité<br>Obesity promotes the development of chronic bronchial diseases (asthma, COPD) and complicates their management, induces sleep breathing disorders and increases susceptibility to respiratory infections. Adipocytea are a source of mediator production including adipokines. Among these, adiponectin (APN) is a 30kDa protein that can associate in multimers of variable molecular weight. It circulates at high level but its serum concentration decreases with weight gain. APN is involved in immunoregulation and pulmonary development. But the pro or anti-inflammatory role of the APN is still a matter for debate. The association between serum levels of APN and the occurrence of bronchial diseases is not clearly demonstrated in humans. We explored the role of adipokines within the respiratory system. In particular, we studied the effect of the APN on the production of cytokines by pulmonary macrophages and bronchial epithelial cells. We obtained lung specimens from patients operated for carcinoma, from which we carried out primary cultures of parenchymal explants, pulmonary macrophages or bronchial epithelial cells and we also prepared bronchial rings for study in organ bath. We have revealed an in situ production of APN by human lung tissue, which is correlated with patient weight. We have verified that APN receptors (AdipoR1 and AdipR2) were both expressed by pulmonary macrophages, bronchial explants, and bronchial epithelial cells. We have treated human lung macrophages with APN (3-10-30 μg/ml) before stimulation with LPS (10 ng / ml) or Poly I: C (10 ng/ml) or IL-4 (10 ng/ml).We have shown that the APN decreased the production of M1 cytokines induced by LPS and Poly I: C (IL-6, CCL3, CCL4, CCL5, CXCL8, TNFa) as well as those of M2 cytokines induced by IL-4 (CCL13, CCL18, CCL22). AdipoRon, a synthetic adiponectin receptor agonist, exhibited the same effects as the recombinant protein. In comparison, leptin at its highest concentration (1000 ng/ml) induced the production of M1-type cytokines (IL-6, CCL3, CCL4, CCL5, TNF-α) by unstimulated macrophages whereas visfatin and chemerin did not reveal any effect on cytokine production by macrophages. Only APN demonstrated an effect on bronchial epithelial cells: decreasing the production of CXCL1 and CCL2 at basal state and after stimulationwith TNF (50 ng / ml) but increasing production of IL6, CCL20 and CXCL8 in the basal situation. We have completed this work by experiments on the regulation of bronchial tone by adipokines, using bronchial rings in isolated organ baths. These results have been the subject of a European patent application. This work is the first looking at the effect of APN and AdipoRon on primary human pulmonary macrophages and bronchial epithelial cells. APN is able to modulate the polarization of these cells. Adipokines are essential for understanding the respiratory burden of obesity
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Dubois, Virginie. "Obésité et cancer mammaire : implication du microenvironnement adipocytaire et des adipokines ?" Thesis, Clermont-Ferrand 1, 2012. http://www.theses.fr/2012CLF1PP01.
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L'obésité est actuellement considérée, d'une part, comme un facteur de risque de développement du cancer du sein en post-ménopause et, d'autre part, comme un facteur de risque de mortalité faisant suite à cette pathologie. Parmi les différentes hypothèses permettant d'expliquer le lien entre obésité et cancer du sein, il est suggéré que les sécrétions adipocytaires (i.e. les adipokines), dont les taux plasmatiques sont connus pour être modulés en situation d'obésité, jouent un rôle important. L'objectif de ce travail de thèse a donc consisté à évaluer l'impact des sécrétions adipocytaires globales et d'adipokines d'intérêt afin de mieux comprendre l'implication potentielle du microenvironnement tumoral adipocytaire sur les phénomènes de cancérogenèse mammaire. Dans une première partie, afin de resituer l'expression protéique de plusieurs adipokines d'intérêt dans l'ensemble complexe des perturbations engageant la cellule tumorale, nous avons mis en relation l'expression de ces adipokines entre elles et avec celle de biomarqueurs connus du cancer du sein (récepteurs aux œstrogènes et à la progestérone, Bax, Bcl2,Ki67...). Pour cela, nous avons comparé, sur des prélèvements mammaires tumoraux et normaux, l'expression de la leptine, de l'adiponectine et de la zinc-α2-glycoprotéine (ZAG). Les tissus cancéreux ou avoisinant la tumeur expriment la leptine et la ZAG et, plus faiblement l'adiponectine, alors que l'expression de ces adipokines n'est pas retrouvée au niveau du tissu sain de femmes non malades. De plus, l'expression de la ZAG et de la leptine est corrélée positivement à celle des récepteurs aux œstrogènes, suggérant qu'il existe un lien étroit entre les voies adipokinique et œstrogénique. Dans une seconde partie, nous avons évalué in vitro, d'une part, le rôle des sécrétions adipocytaires globales, grâce à la mise en place d'un modèle original de «derme adipeux tridimensionnel» épithélialisé en présence des cellules mammaires, fibrokystiques ou tumorales, et, d'autre part, l'impact d'adipokines d'intérêt (leptine et ZAG) sur différentes lignées de cellules mammaires cancéreuses. Nous avons montré qu'il existe un dialogue réciproque entre le microenvironnement adipeux et les cellules mammaires cancéreuses, favorisant la croissance tumorale. Nous avons également établi que la leptine et la ZAG exercent des effets prolifératifs et anti-apoptotiques. Dans une troisième partie, nous avons cherché à mieux comprendre le fait que l'obésité augmente le risque de mortalité due au cancer du sein, en émettant deux hypothèses complémentaires : i) il pourrait y avoir une moindre efficacité des traitements d'hormonothérapie et/ou de chimiothérapie en cas d'obésité liée à une interférence avec certaines adipokines,et ii) il pourrait exister un risque accru d'apparition de métastases provenant notamment d'une influence des adipokines sur les processus angiogéniques. Ainsi, in vitro, nous avons montré que la leptine diminue l'efficacité de plusieurs traitements anti-cancéreux et augmente les processus angiogéniques et d'invasion tumorale, notamment quand elle est utilisée à des concentrations reflétant une imprégnation plasmatique en situation d'obésité, alors que l'adiponectine inhibe l'angiogenèse pour des concentrations reflétant l'imprégnation plasmatique en situation physiologique. Nos résultats suggèrent que les sécrétions adipocytaires sont impliquées dans la régulation du développement du tissu cancéreux au niveau mammaire et laissent entrevoir des pistes prometteuses concernant le ciblage des adipokines dans la prévention et/ou le traitement de la pathologie cancéreuse mammaire, plus particulièrement en cas de surcharge pondérale<br>Obesity is now considered, firstly, as a risk factor for developing breast cancer in postmenopausal women and, secondly, as a risk factor for mortality in response to this pathology. Among the various hypotheses to explain the link between obesity and breast cancer, it is suggested that the adipocyte secretions (ie adipokines), whose plasma levels are known to be modulated in obesity are important. The objective of this work was therefore to assess the overall impact of adipocyte secretions and adipokines of interest to better understand the potential involvement of adipocyte tumor microenvironment in mammary carcinogenesis. In the first part, in order to situate the protein expression of several adipokines of interest in the complex disturbances involving the tumor cell, we have related the expression of these adipokines together and with that of more classical biomarkers of breast cancer (estrogen and progesterone receptor, Bax, Bcl2, Ki67...). For this, we compared, on mammary tumor and normal samples, the expression of leptin, adiponectin and zinc-α2-glycoprotein (ZAG). Cancerous tissue or normal tissue surrounding the tumor express leptin and ZAG and, more weakly, adiponectin, whereas expression of leptin and ZAG is not found in healthy tissue from women without disease. Furthermore, the expression of ZAG and leptin is positively correlated with that of the estrogen receptor, suggesting that there is a close connection between the adipokine and estrogen pathways. In the second part, we evaluated in vitro, on the one hand, the role of overall adipocyte secretions, through the establishment of an original model of "three-dimensional dermis fat" epithelialized in the presence of mammary cells, tumor or fibrocystic, and,on the other hand, the impact of interest adipokines (leptin and ZAG), on different lines of breast cancer cells. We have shown that there is a reciprocal dialogue between the adipose microenvironment and breast cancer cells, promoting tumor growth. Wealso found that leptin and ZAG exert proliferative and anti-apoptotic effects. In the third part, we try to understand the fact that obesity increases the risk of mortality from breast cancer, by issuing two additional assumptions :i) there may be a less effective treatment in situation of obesity related to an interference with some adipokines, and ii) there may be an increased risk of metastasis due to an influence of adipokines on the angiogenic process. Thus, in vitro, we showed that leptin decreases the efficacy of several cancer treatments and increases the angiogenic process and tumor invasion, especially when leptin is used at concentrations reflecting plasma impregnation in a situation of obesity, while adiponectin inhibits angiogenesis, particularly for concentrations reflecting impregnation in plasma in physiological situation. Our results suggest that adipocyte secretions are involved in regulating of breast cancer development and suggest promising ways for targeting adipokines in the prevention and / or treatment of breast cancer pathology, especially in case of overload weight
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Martins, Leandro de Mattos Boer 1978. "Variabilidade da função autonômica em pacientes com hipertensão arterial resistente." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309565.
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Previous issue date: 2011<br>Resumo: Considerando a forte associação entre a atividade do sistema nervoso autônomo, a obesidade e a resistência insulínica na hipertensão arterial resistente (HAR), esta pesquisa teve a finalidade de identificar a associação entre a função do sistema nervoso autonômico e importantes hormônios relacionados à síndrome cardiometabólica como adiponectina, leptina e aldosterona. Vinte e cinco pacientes portadores de hipertensão arterial resistente foram divididos em dois grupos: com (DM2) e sem diabetes mellitus tipo 2 (NDM2). Ambos os grupos foram avaliados em relação à variabilidade da frequência cardíaca (VFC) pelo sistema Holter de 24 horas, nos domínios do tempo e da frequência, e aos hormônios plasmáticos adiponectina, leptina e aldosterona. A análise dos resultados demonstrou maior disfunção autonômica e hipoadiponectinemia no subgrupo DM2 em relação ao subgrupo NDM2, correlação positiva entre VFC no domínio do tempo e a adiponectina no total de pacientes, ruptura do ritmo circadiano de ambos os grupos (tônus simpático aumentado no período noturno e diminuído no período diurno; tônus parassimpático aumentado no período diurno e diminuído no período noturno) e correlação positiva entre a banda de baixa de frequência em unidades normalizadas (LFnu) e aldosterona, e correlação negativa entre a banda de alta frequência em unidades normalizadas (HFnu) e aldosterona no total de pacientes e em ambos os grupos. O grupo DM2 obteve maiores valores de leptina e índice de massa corporal. Entretanto, não houve correlação entre a VFC e leptina em ambos os grupos. Desta forma, identificou-se ruptura do ritmo circadiano e a associação entre o balanço autonômico e os níveis de adiponectina e aldosterona plasmática na HAR com e sem diabetes tipo 2<br>Abstract: Considering the strong association between the autonomic nervous system activity, obesity and insulin resistance in resistant hypertension (RH), this research aimed to identify the association of the autonomic nervous system function and important hormones related to the cardiometabolic syndrome such as adiponectin, leptin and aldosterone. Twenty five RH patients were divided into two groups: with (T2D) and without type-2 diabetes (NT2D). Both groups were evaluated regarding the heart rate variability (HRV) by the Holter system in 24 hours, in time and frequency domains, and the plasma hormones adiponectin, leptin and aldosterone. The analysis of the results demonstrated greater autonomic dysfunction and hypoadiponectinemia in T2D subgroup compared to the NT2D subgroup, positive correlation between HRV in time domain and adiponectin in all patients, circadian disruption in both groups (increased sympathetic drive during nighttime and decreased during daytime; increased parasympathetic drive during daytime and decreased during nighttime) and positive correlation between the low frequency band in normalized units (LFnu) and aldosterone, and negative correlation between the high frequency band in normalized units (HFnu) and aldosterone in all patients and both subgroups. The T2D subgroup had higher levels of leptin and body mass index. However, there was no correlation between HRV and leptin in both groups. Thereby, it was found circadian disruption and the relationship between autonomic balance and plasma adiponectin and aldosterone in RH with or without type 2 diabetes<br>Doutorado<br>Doutor em Farmacologia
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Nunes, Marina. "Influência de diferentes ambientes intrauterinos sobre a composição hormonal do colostro e leite maduro e o peso de lactentes : coorte ivapsa." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/118286.
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Objetivo: Avaliar a influência de diferentes ambientes intrauterinos na concentração de hormônios no leite materno e sua relação com o peso da criança nos primeiros seis meses de vida. Materiais e Métodos: Trata-se de um de estudo de coorte prospectivo de uma amostra de recém-nascidos a termo da cidade de Porto Alegre. O recrutamento dos pares mãe-bebê ocorria 24 a 48 horas após o parto e os sujeitos incluídos em um dos cinco grupos: Diabetes, Hipertensão, Tabagistas, Pequenos para Idade Gestacional (PIG) e Controle. O colostro foi coletado no pós-parto e o leite maduro no 1º mês. Foram quantificadas as concentrações de Leptina, Adiponectina e Insulina pelo método ELISA. O peso e a estatura das mães e das crianças foram obtidos em todas as entrevistas Resultados: A concentração dos hormônios diminuiu com a maturação do leite materno com diferença estatística do colostro para o leite maduro para leptina no PIG (p=0,05) e Insulina nos grupos PIG (p=0,012) e Controle (p=0,041). O grupo PIG diferiu estatisticamente do Controle na concentração de leptina no 1M (p=0,045). O peso dos recém-nascidos PIG foi inferior aos outros grupos no nascimento e na alta hospitalar, mantendo-se diferente aos 15 dias do diabetes e controle, e, apenas do controle, no 1º mês. A partir dessa entrevista, a média de peso do PIG foi semelhante aos outros grupos indicando um catch up precoce avaliado pela diferença de escore-Z de peso para idade (>0,67). Tanto a leptina (r=-0,295; p=0,03) quanto a insulina (r=0,262; p=0,047) do leite maduro se correlacionaram com o ganho de peso da criança no 1º mês. Conclusões: A concentração dos hormônios no leite materno dos cinco grupos é semelhante ao nascimento, mas diminui do colostro para o leite maduro. A leptina e a insulina tem redução estatisticamente significativa no grupo PIG. O estudo demonstra uma antecipação metabólica do leite materno sobre a condição de PIG, relacionando-se com a possibilidade de um catch up precoce no primeiro mês de vida desses lactentes.<br>Objective: To evaluate the influence of different intrauterine environments on breast milk hormones concentration and its relationship with infant weight up to 6 months. Material and Methods: This is a thematic, prospective and longitudinal term born cohort from Porto Alegre, Brazil. Mother-infant pairs were recruited 24 to 48 hours after birth and then included in one of five groups: diabetes, hypertension, smoking, mothers of Small for Gestational Age (SGA) and controls. Colostrum was collected at 24h postpartum and mature milk 1 month later. Breast milk leptin, adiponectin and insulin were determined by ELISA. In all interviews mother and infant weight and height were obtained. Results: Adipokines levels decreased according to milk maturation with statistical difference in leptin from colostrum to mature milk in SGA group (p=0.05) and insulin in SGA (p=0.012) and control (p=0.041) groups. SGA differed statistically from control at colostrum in leptin concentration (p=0,045). SGA had low maternal BMI means values in all measurements reflecting in lower leptin and insulin concentration. SGA infant weight was statistically different from all groups at born and at discharge keeping different from diabetes and control at 15 days postpartum and only from control at 1 month. After, the weight mean of SGA was similar from others groups indicating an early catch up. Both, leptin (r=-0.295; p=0.03) and insulin (r=0.262; p=0.047) at 1 month were correlated with infant weight gain at 1 month. Conclusion: Breast milk hormones are similar at birth in all groups but the concentration decreases from colostrum to mature milk. SGA had a significant reduction in leptin and insulin concentration. This study demonstrates breast milk metabolic anticipation on SGA, probably is related to early catch up at 1 month of life.
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Oliveira, Gustavo Bernardes de Figueiredo. "Adiponectina, perfil metabólico e risco cardiovascular em pacientes com síndromes coronarianas agudas." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/98/98131/tde-19092011-080932/.
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O tecido adiposo é considerado não somente uma fonte de energia estocável, mas principalmente um órgão endócrino que secreta várias citoquinas, as quais podem contribuir para o desenvolvimento de doenças relacionadas à obesidade, incluindo o diabetes mellitus e a doença vascular aterosclerótica. Dentre esse pool de moléculas, a adiponectina (Arcp30, AdipoQ, apM1, ou GBP28), uma nova proteína semelhante ao colágeno, foi descoberta como uma citoquina específica do adipócito. Neste estudo, realizamos a determinação dos níveis séricos da adiponectina em uma amostra de pacientes hospitalizados com SCA e, posteriormente, avaliamos a associação com os eventos cardiovasculares no seguimento clínico. Método: avaliamos 114 pacientes com SCA de ambos os sexos neste estudo de corte transversa com seguimento clínico mediano de 18 meses. Realizamos análise de regressão multivariada de Cox para identificar associação independente entre adiponectina e o risco subsequente de óbito CV, IAM não-fatal, AVE não-fatal, e rehospitalização com revascularização. Também comparamos os diversos biomarcadores metabólicos, inflamatórios, de coagulação e de necrose miocárdica por quartis de adiponectina. Resultados: Adiponectina não correlacionou-se de modo independente com o risco CV, tanto na análise univariada quanto nos modelos de Cox. Das variáveis metabólicas, a única com valor preditivo para os desfechos primário e co-primário foi a glicemia de jejum, com OR ajustado=1,06 (IC95% 1,01-1,11), p=0,016, e OR ajustado=1,10 (IC95% 1,03-1,17), p=0,003, ambos para incrementos de 10 na glicemia de jejum. Conclusões: Adiponectina não se mostrou variável independente de risco cardiovascular nesta amostra de pacientes com SCA. A glicemia de jejum foi a única variável metabólica com valor preditivo independente para os desfechos cardiovasculares.<br>Background: The adipose tissue is considered not only an energy resource stock, but mainly an endocrine organ that secretes several cytokines, which may contribute to the development of diseases related to obesity, including diabetes mellitus and the atherosclerotic vascular diseases. Within this pool of molecules, adiponectin (Arcp30, AdipoQ, apM1, or GBP28), a novel protein similar to collagen, was discovered as an adipocyte-specific cytokine. In this study, we determined the serum levels of adiponectin in a sample of patients hospitalized with acute coronary syndromes (ACS), and subsequently we evaluated the association with the cardiovascular events during the follow-up phase. Methods: we evaluated 114 patients with ACS of both genders in this cross-sectional study with a median follow-up of 18 months. We performed a proportional multiple regression analysis of Cox to identify independent association between adiponectina and risk of cardiovascular death, non-fatal acute MI, non-fatal CVA, and rehospitalization requiring revascularization. We also compared the various biomarkers of metabolism, inflammation, coagulation, and of myocardial necrosis divided by quartiles of adiponectin. Results: Adiponectin did not correlate independently with CV risk, either on univariate analysis or on the multiple regression models of Cox. Among the metabolic biomarkers, the only variable with predictive value for the primary and co-primary endpoints was fasting glucose, with an adjusted OR=1,06 (95%CI 1,01-1,11), p=0,016, and adjusted OR=1,10 (95%CI 1,03-1,17), p=0,003, both for increments of 10. Conclusions: Adiponectin was not an independent risk factor for cardiovascular risk in this sample of ACS patients. Fasting glucose was the only metabolic biomarker with a significant and independent predictive value for cardiovascular outcomes.
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Madeira, Isabel Rey. "Leptina, adiponectina, resistência insulínica e componentes da Síndrome Metabólica em crianças pré-púberes com excesso de peso." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3430.
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Obesidade, hipertensão arterial, dislipidemia e metabolismo glicídico alterado são fatores de risco cardiovascular, reunidos sob a sigla síndrome metabólica (SM), onde a resistência insulínica tem papel central. Estes fatores já atuariam na infância. São objetivos desta pesquisa: determinar, por intermédio de pontos de corte de HOMA-IR descritos na literatura, aquele que mais bem identifique SM em crianças pré-púberes obesas e com sobrepeso; verificar o impacto da obesidade sobre componentes da SM e sobre níveis de leptina e adiponectina em crianças pré-úberes; determinar o papel dos componentes da SM, da leptina e da adiponectina na resistência insulínica nestas crianças. Realizou-se estudo transversal com 112 crianças pré-púberes obesas, 36 com sobrepeso e 49 eutróficas, oriundas do ambulatório de pediatria geral do HUPE-UERJ. Para o primeiro objetivo, nas obesas e com sobrepeso, estimaram-se sensibilidade e especificidade para cada ponto de corte de HOMA-IR tomando-se como desfecho SM. Uma curva receiver operating characteristic foi construída com estes valores. Para o segundo objetivo, 30 crianças obesas, 31 com sobrepeso e 33 eutróficas foram comparadas quanto às médias de glicose (G), lipídios, insulina (I), HOMA-IR, relação G/I, adiponectina e leptina; compararam-se as freqüências de acantose nígricans e das alterações de cintura, pressão arterial, G, lipídios séricos e I; avaliou-se a correlação entre escore Z de IMC (ZIMC) e adipocitoquinas. Para o terceiro objetivo, compararam-se crianças com e sem resistência insulínica quanto às médias de idade, ZIMC, lipídios, leptina e adiponectina; compararam-se também as freqüências de sexo, circunferência da cintura aumentada, hipertensão arterial e acantose nígricans; estudou-se correlação das variáveis com HOMA-IR (regressão linear múltipla), e associação destas com resistência insulínica (regressão logística). O ponto de corte de HOMA-IR que melhor identificou a SM foi 2,5 (sensibilidade=61%; especificidade=74%). Na comparação de crianças obesas, com sobrepeso e eutróficas, houve diferença nas médias dos obesos quanto a HDL-colesterol e adiponectina (médias menores), e nas dos eutróficos quanto a I, HOMA-IR, relação G/I e leptina (médias menores) (p<0,001); o mesmo em relação às freqüências dos obesos quanto a acantose nígricans e alteração de cintura e HDL-colesterol (freqüências maiores) (p<0,005); o ZIMC se correlacionou positivamente com leptina (p<0,001) e negativamente com adiponectina (p=0,001); na regressão linear múltipla, esta correlação se manteve apenas para leptina. Ao se comparar as crianças com e sem resistência insulínica, houve diferença nas médias de idade, ZIMC, HDL-colesterol, triglicerídeos, leptina e adiponectina (p<0,01) e nas freqüências de acantose nígricans e circunferência da cintura aumentada (p<0,005); houve correlação positiva entre idade, triglicerídeos, leptina, sexo (feminino) e acantose nígricans com HOMA-IR (regressão linear múltipla) (p<0,05), e associação positiva de idade, triglicerídeos, leptina e sexo (feminino) com resistência insulínica (regressão logística) (p<0,05). O índice HOMA-IR pode ser útil para detectar SM, e o ponto de corte 2,5 mostrou-se o melhor. Os achados comprovam a influência da obesidade sobre os componentes da SM e sobre os níveis de adipocitoquinas já nas crianças pré-púberes e apontam para a importância destas na gênese da doença cardiovascular. Dentre os componentes da SM, destacou-se o papel dos lipídios na resistência insulínica. Também se mostraram importantes acantose nígricans, leptina e adiponectina.<br>Obesity, hypertension, dyslipidemia and impaired glucose metabolism are cardiovascular risk factors, congregated under the title metabolic syndrome (MS), were insulin resistance has central role. The aims of this work are: to establish, among the cut-off values for HOMA-IR cited in the literature, the best in identifying MS in obese and overweight prepubertal children; to verify the obesity impact on MS components, leptin and adiponectin levels in prepubertal children; to verify the role of MS components, leptin and adiponectin in insulin resistance among these children. The cross-sectional work studied 112 obese, 36 overweight and 49 eutrophic prepubertal children attending the HUPE-UERJ outpatient pediatric clinic. For the first objective, it was estimated sensibility and specificity for MS of each cut off-point of HOMA-IR. A receiver operating characteristic curve was generated using these values. For the second objective, it was compared: the means of glucose (G), lipids, insulin (I), HOMA-IR, G/I relation, leptin and adiponectin from 30 obese, 31 overweight and 33 eutrophic children; the frequencies of acantosis nigricans and changes in waist, blood pressure, glucose, lipids and insulin; the correlation between body mass index z score (BMIz) and adipokines was evaluated. For the third objective, it was compared: the means of age, BMIz, lipids, leptin and adiponectin among children with and without insulin resistance; the frequencies of sex, increased waist circumference, hypertension and acantose nígricans; the correlation between those variables with HOMA-IR (multiple linear regression) and the association of them with insulin resistance (logistic regression) were evaluated. The best cut-off value of HOMA-IR for MS was 2.5 (sensibility=61%; specificity=74%). In the comparison between obese, overweight and eutrophic children, the obese differed from the others in the mean values of HDL-cholesterol and adiponectina (smaller mean values), whereas the eutrophic children differed in the mean values of I, HOMA-IR, G/I relation, and leptin (smaller mean values) (p<0.001); it was observed the same regarding the frequencies of acantose nigricans and alteration in waist and HDL-cholesterol in the obese (higher frequencies) (p<0.005); the BMIz showed a positive correlation with leptin (p<0.001) and a negative correlation with adiponectin (p=0.001); in multiple linear regression, this correlation was maintained only for leptin. In the comparison between children with and without insulin resistance, there was difference regarding the mean values of age, BMIz, HDL-cholesterol, triglycerides, leptin and adiponectina (p<0.01), and regarding the frequencies of acantose nigricans and increased waist circumference (p<0.005); in multiple linear regression age, triglycerides, leptin, sex (feminine) and acantose nigricans showed positive correlation with HOMA-IR (p<0.05), and in logistic regression, age, triglycerides, leptin and sex (feminine) showed positive association with insulin resistance (p<0.05). HOMA-IR may be useful to detect MS and the cut-off 2.5 seems to be the best. The finds provide evidence of the influence of obesity on MS components and on adipokine levels in prepbertal children, indicating that these components may contribute to the beginning of cardiovascular disease. Among the MS components, the lipids had prominent place in insulin resistance. Acantose nigricans, leptin and adiponectin also showed importance.
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Nogues, Perrine. "Impact de l’obésité maternelle sur les fonctions placentaires : rôles de la leptine et de l'adiponectine Maternal obesity alters placental nutrient transport associated with inflammatory status and morphology modifications in human term placenta Maternal obesity influences expression and DNA methylation of the adiponectin and leptin systems in human third-trimester placenta." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLV101.
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L’obésité se définit par une accumulation excessive de masse grasse et une inflammation systémique chronique. Elle se mesure par un indice de masse corporelle supérieur à 30 kg/m². L’obésité maternelle est associée à de nombreux troubles de la santé et en particulier à un risque accru de développer des pathologies de la grossesse (pré éclampsie, diabète gestationnel). D’autre part, l’obésité maternelle impacte la descendance avec une augmentation des risques d’apparition de maladies métaboliques à l’âge adulte.Le placenta est un organe présent à l’interface entre la mère et le fœtus. Il assure des fonctions endocrines, d’échanges et de protection immunitaire.La leptine et l’adiponectine sont des adipokines majoritairement produites par le tissu adipeux. La leptine joue un rôle satiétogène et l’adiponectine exerce des effets insulino-sensibilisateurs. Elles sont donc impliquées dans l’homéostasie énergétique.Le placenta exprime la leptine et les récepteurs spécifiques de ces deux hormones. Il est bien établi que la leptine et l’adiponectine participent au contrôle des fonctions placentaires.Au cours de ce travail, nous nous sommes intéressés à l’impact de l’obésité maternelle (sans diabète gestationnel) sur les principales fonctions du placenta humain.Dans une première partie, nous avons montré que l’obésité maternelle entraîne i) une diminution de l’expression des transporteurs de nutriments, ii) une diminution du nombre de cellules immunitaires, iii) une altération des capillaires fœtaux et iv) une diminution de la production de cytokines pro-inflammatoires et de l’hormone chorionique gonadotrope (hCG) dans le placenta à terme.Dans une deuxième partie, nous avons montré que l’obésité maternelle altère l’expression des systèmes leptine et adiponectine (ligand et récepteurs) dans le placenta humain. En effet, l’obésité maternelle conduit à une diminution de l’expression des récepteurs des deux hormones et à une modification de la méthylation des régions promotrices des gènes codant pour les deux adipokines et leurs récepteurs.L’ensemble de ces résultats montre que l’obésité maternelle altère les fonctions endocrines, d’échanges et immunitaires du placenta. Cet organe transitoire semble s’adapter à un environnement maternel délétère<br>This research investigates the impact of maternal obesity without gestational diabetes on the major functions of the human placenta. Obesity is defined as an excessive accumulation of fat mass and chronic low grade inflammation. Obesity is indicated by a body mass index (BMI) higher than 30 m2/kg. Maternal obesity is associated with health disorders and creates a higher risk for the development of pregnancy complications (pre-eclampsia and gestational diabetes). In addition to obesity having an impact on a pregnant woman, the fetus is also at risk of developing metabolic disorders in adulthood.The placenta is the organ present at the interface between the mother and the fetus. The placenta’s role is to ensure endocrine functions, exchange functions, and immune protection.Leptin and adiponectin are mostly produced by the adipose tissue. Leptin is a key player in satiety, whereas adiponectin displays an insulin-sensitizing effect. Therefore, both are involved in the energy homeostasis and both are well-established as being involved in the control of placental functions.In this research, we investigated the impact of maternal obesity (without gestational diabetes) on the major functions of the human placenta.In a first part, we have shown that maternal obesity leads to i) a lower expression of nutrient transporters, ii) a lower count of immune cells, iii) an alteration of fetal capillaries, and iv) a decrease in the production of pro-inflammatory cytokines and gonadotropic chorionic hormone (hCG) in term placenta.Also covered in this research is that maternal obesity impairs the leptin and adiponectin systems (ligand and receptors) in the human placenta. Our results indicate maternal obesity is associated with a lower expression of the two adipokines receptors; as well as to a modification in the DNA methylation of promoter regions of the genes’ coding for the two hormones and their receptors.The conclusion of the research reveals how maternal obesity affects the endocrine, exchange, and immune functions of the placenta and how this transient organ seems to adapt itself to a harmful maternal environment
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Schaarschmidt, Wiebke [Verfasser], Matthias [Akademischer Betreuer] Blüher, Gerhard [Gutachter] Schuler, and Martin [Gutachter] Busse. "Auswirkungen eines zwölfmonatigen kontrollierten Trainingsprogramms auf die Leptin-, Adiponectin- und Progranulin-Serumkonzentrationen sowie Parameter des Lipidstoffwechsels bei Patienten mit Typ 2 Diabetes / Wiebke Schaarschmidt ; Gutachter: Gerhard Schuler, Martin Busse ; Betreuer: Matthias Blüher." Leipzig : Universitätsbibliothek Leipzig, 2011. http://d-nb.info/1237895936/34.
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Martins, Cyro José de Moraes. "Associação do sistema leptina e adiponectina com fatores de risco cardiometabólico em população de origem multiétnica com variados graus de adiposidade." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1436.
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O objetivo desse estudo foi avaliar a associação das adipocitocinas (sistema leptina e adiponectina) com fatores de risco cardiometabólico, grau de resistência insulínica e fenótipo de síndrome metabólica em uma população de origem multiétnica com variados graus de adiposidade. O sistema leptina é constituído pela leptina plasmática, receptor solúvel de leptina e índice de leptina livre, este último calculado como a razão entre a leptina e seu receptor solúvel. Cento e setenta e três indivíduos (idade, 45 12 anos; 124 mulheres; índice de massa corporal, 35,6 9,5 kg/m2) foram selecionados entre 310 participantes de um estudo sobre marcadores genéticos de fatores de risco cardiometabólico, e avaliados do ponto de vista antropométrico, hemodinâmico e laboratorial, para determinar o seu perfil metabólico e as concentrações de adiponectina, leptina e receptor solúvel de leptina. Os níveis de leptina mostraram correlação inversa com as concentrações de seu receptor solúvel, porém a adiponectina não mostrou associação significativa com o sistema leptina. A leptina e o índice de leptina livre se associaram positivamente com os fatores de risco cardiometabólico (P ≤ 0,006), exceto colesterol total, e negativamente com o HDL-colesterol (P ≤ 0,005), ao contrário do receptor solúvel da leptina, que exibiu relação inversa com os fatores de risco (P < 0,001), exceto glicose e parâmetros lipídicos. A adiponectina associou-se inversamente com a relação cintura/quadril, HOMA-IR e concentração plasmática de insulina (P ≤ 0,005). Os valores de leptina e índice de leptina livre aumentaram, e de receptor solúvel diminuíram ao longo dos tercis de índice de massa corporal, circunferência da cintura, relação cintura/quadril, pressão arterial sistólica, HOMA-IR e também com o aumento no número de componentes da síndrome metabólica (P para tendência <0,05). Em modelos multivariáveis, sexo, índice de massa corporal e insulina mostraram associação independente com leptina e índice de leptina livre, ao passo que idade, sexo, índice de massa corporal e pressão arterial sistólica apresentaram associação independente com o receptor solúvel de leptina. Ao felacionar conjuntamente as adipocitocinas, somente leptina demonstrou associação independente com a síndrome metabólica (odds ratio: 3,35; intervalo de confiança de 95%: 1,90 - 5,91; P < 0,001). Nessa população multiétnica, o sistema leptina e a adiponectina mostraram associação com os fatores de risco cardiometabólico, o grau de resistência insulínica e o fenótipo da síndrome metabólica.<br>The aim of this study was the assessment of the cross-sectional associations of the adipokines (leptin system and adiponectin) with cardiometabolic risk factors, insulin resistance and the metabolic syndrome phenotype in a multiethnic population with varying degrees of adiposity. The leptin system consists of plasma leptin, soluble leptin receptor and the free leptin index, calculated as the ratio of the concentrations of leptin and soluble leptin receptor. One hundred and seventy three subjects (aged 4512 years; 124 women; body mass index 35.69.5 kg/m2) were selected among 310 individuals referred to participate in a study on genetic markers of cardiometabolic risk factors. Blood samples were assessed for metabolic profile, adiponectin, leptin and its soluble receptor levels. Leptin and soluble leptin receptor were inversely correlated, but adiponectin was not significantly correlated with the other adipokines. Leptin and free leptin index were positively associated with cardiometabolic risk factors, except for total cholesterol; contrariwise, both variables were inversely related to HDL-cholesterol. Soluble leptin receptor exhibited an inverse relation to cardiometabolic risk factors, except for plasma glucose and lipid parameters (P ≤ 0.006 for all cases). Adiponectin was inversely related to waist-to-hip ratio, homeostasis model assessment index, and insulin (P ≤ 0.005 for all cases). Leptin and free leptin index increased, whereas soluble leptin receptor decreased across tertiles of body mass index, waist circumference, waist-to-hip ratio, systolic blood pressure, homeostasis model assessment index and with increasing number of metabolic syndrome components (P for trend < 0.05 for all cases). In multivariable models, sex, body mass index and insulin were independently associated with leptin and free leptin index, whereas age, sex, body mass index and systolic blood pressure were the independent correlates of soluble leptin receptor. Relating all adipokines conjointly to metabolic syndrome, only leptin demonstrated independent association with the phenotype (odds ratio, 3.35; 95% confidence interval, 1.90 - 5.91; P < 0.001). In this multiethnic population, the leptin system and adiponectin were associated with cardiometabolic risk factors, insulin resistance and the metabolic syndrome phenotype.
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Zelenskiy, Svetlana. "Effect of dietary glycemic load and single nucleotide polymorphisms in the adipogenesis pathway on colon cancer susceptibility." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1386349030.
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Rönn, Monika. "Environmental Contaminants and Obesity." Doctoral thesis, Uppsala universitet, Arbets- och miljömedicin, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-209807.
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Obesity is a worldwide problem affecting both children and adults. Genetic, physiological, environmental, psychological, social and economic factors interact in varying degrees, influencing body weight and fat distribution and the progress of obesity. Moreover, some anthropogenic chemicals have proven to be endocrine disrupting chemicals (EDCs) with the potential to interfere with different actions of hormones in the body. EDCs may thereby disrupt homeostasis, modifying developmental, behavioral and immune functions in humans and animals, and also promoting adiposity. Because hormones generally act at low concentrations, small changes in the endocrine system may lead to extensive effects. Based on data from experimental and epidemiological studies this thesis elucidates the relationship between a large number of environmental contaminants and obesity. The experimental studies demonstrated that fructose supplementation in the drinking water resulted in unfavorable metabolic alterations such as a higher liver somatic index (LSI), an increase in plasma triglycerides and increased plasma levels of apo A-I. Fructose in combination with exposure to bisphenol A (BPA) increased liver fat content and plasma levels of apo A-I in juvenile female Fischer 344 rats. The experimental studies also showed that the retro-peritoneal fat, which in rats is a distinct fat depot easy to distinguish and dissect, correlated well with the measurements of total fat mass analyzed with MRI, and could therefore be used as a substitute for total fat mass in rats. The epidemiological studies showed that circulating levels of persistent organic pollutants (POPs) were related to fat mass measured by DXA. OCDD, HCB, TNC, DDE and the less chlorinated PCBs were positively related to fat mass, while the more highly chlorinated PCBs showed a negative association. Further, circulating levels of BPA were positively associated with levels of the hormones adiponectin and leptin, but negatively related with ghrelin, hormones which are involved in the regulation of hunger and satiety. However, serum BPA levels were not related to measures of fat mass in the elderly individuals in the PIVUS cohort. This thesis concludes that environmental contaminants such as BPA and POPs most likely are contributors, along with genetic, social and behavioral factors, to the development of obesity.
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Houde, Andrée-Anne. "Programmation métabolique foetale : étude de l'impact de l'exposition au diabète gestationnel sur le méthylome du nouveau-né." Thèse, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6851.
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Résumé : L’obésité est un enjeu de société de première importance; elle est un facteur de risque de plusieurs maladies et engendre d’importantes dépenses en santé. Outre l’alimentation, la sédentarité et les prédispositions génétiques, il semble que l’environnement fœtal soit un facteur déterminant dans le développement de l’obésité. En effet, il a été démontré que les nouveau-nés exposés à un environnement intra-utérin défavorable ont un risque accru de développer, à l’adolescence et à l’âge adulte, l’obésité ainsi que les désordres métaboliques qui y sont associés. Le diabète gestationnel (DG) est l’une des complications de santé maternelle les plus fréquentes et est associé à un risque accru à long terme pour la santé métabolique de l’enfant. Malgré les nombreuses données probantes épidémiologiques concernant le phénomène de la programmation fœtale associée au DG, les mécanismes moléculaires impliqués ont été très peu étudiés. Il est cependant de plus en plus évident que l’épigénétique soit l’un de ces mécanismes. Cette thèse a pour objectif d’identifier les changements de méthylation de l’ADN, la modification épigénétique la plus stable et la plus connue, chez les nouveau-nés exposés in utero au DG. Dans un premier temps, la méthylation de l’ADN de 44 échantillons de placenta et de sang de cordon a été analysée à l’échelle du génome. Cette approche a permis de démontrer que les gènes épigénétiquement modifiés suite à une exposition au DG sont majoritairement retrouvés dans les voies biologiques associées aux maladies métaboliques. Des analyses dans une cohorte indépendante (n=80) ont confirmé l’effet de la glycémie maternelle sur la méthylation de l’ADN des gènes BRD2, LRP1B et CACNA1D impliqués dans la régulation du métabolisme des lipides et du glucose et du système rénine-angiotensine respectivement. Dans un second temps, l’approche par gènes candidats a démontré que l’exposition au DG est associée à la méthylation de l’ADN de gènes du métabolisme des lipides (LPL et ABCA1) du placenta. L’analyse de la méthylation de la LEP et de l’ADIPOQ dans le sang et les tissus adipeux de sujets sévèrement obèses a permis d’identifier des sites de méthylation pouvant potentiellement être utilisés dans le sang comme marqueur de susceptibilité à l’obésité. L’ensemble des résultats de cette thèse démontrent que le DG modifie le profil épigénétique de gènes impliqués dans les voies biologiques des maladies métaboliques (métabolisme énergétique et des lipides) et supportent l’importance de la méthylation de l’ADN dans la programmation de la santé métabolique du nouveau-né ayant été exposé in utero au DG.<br>Abstract : Obesity has reached epidemic proportions worldwide in both adult and childhood populations and is now recognized as a major public health issue. Obesity is associated with higher incidence of cardiometabolic complications including type 2 diabetes (T2D), dyslipidemia and hypertension as well as with increased health care costs. The fetal environment now appears, with genetics and the environment, as one cause of the obesity epidemic. Indeed, according to the fetal programming hypothesis, newborns exposed to a detrimental fetal environment are more susceptible to develop obesity, T2D and other related chronic disorders when they become teenagers or adults. Many studies have associated gestational diabetes mellitus (GDM) exposure with these long-term metabolic health risks for the newborn. Although, numerous studies show epidemiological evidence to support the fetal programming hypothesis, only a few studies have been undertaken to understand the underlying molecular mechanisms. However, several studies now suggest that epigenetics may be involved. The objective of this thesis is to study changes in DNA methylation, the more stable and studied epigenetic system, in newborns that have been exposed to GDM in utero. First, a genome-wide DNA methylation analysis (BeadChip) was performed in a sample set of 44 placenta and cord blood samples to identify genes and metabolic pathways dysregulated by GDM. This approach showed that genes epigenetically affected by GDM are predominantly involved in metabolic diseases. The associations between maternal glycemia and DNA methylation levels were confirmed, in an independent birth cohort, for BRD2, LRP1B and CACNA1D gene loci involved in the regulation of lipid and glucose metabolism and the renin-angiotensin system respectively. Then, using a candidate gene approach we reported that DNA methylation levels at gene loci involved in lipid metabolism (LPL and ABCA1) are modified in the placenta following exposure to GDM. Furthermore, analyses of LEP and ADIPOQ DNA methylation levels in blood and adipose tissues of severely obese men and women allowed the identification of CpG sites that might be used in blood as a marker of obesity susceptibility. Altogether the results of this thesis show that GDM affects the epigenetic signature of genes involved in metabolic disease pathways (energy and lipid metabolism) and support the role of DNA methylation in metabolic health programming of the newborn exposed to GDM.
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Araújo, Michella Soares Coelho. "Obesidade e resistência à insulina induzida pela restrição crônica no consumo de sal em ratos Wistar: efeitos sobre o balanço energético, sistema renina-angiotensina (SRA) e sinalização da insulina." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-15012007-134042/.
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A restrição de sal na dieta está associada com resistência à ação da insulina e obesidade. O mecanismo molecular pelo qual a dieta hipossódica (HO) pode induzir resistência à insulina e obesidade não está totalmente compreendido. O objetivo do presente estudo foi avaliar a influência da ingestão crônica de sal sobre o peso corporal (PC), sinalização da insulina no fígado, músculo e tecido adiposo branco (TAB) e sua associação com adiposidade e resistência à insulina. Com esta finalidade, ratos Wistar foram alimentados com dieta HO, normossódica (NR) ou hipersódica (HR) desde o desmame. O PC foi avaliado desde o desmame. Ao completarem 12 semanas de vida, foram avaliados pressão arterial, balanço energético, consumo de ração, glicemia, angiotensina II (ANGIO II) plasmática e perfil hormonal. A atividade motora espontânea foi estudada em ratos com 8 e 12 semanas. A sensibilidade à insulina foi analisada pelo índice de HOMA. A expressão da proteína desacopladora mitocondrial 1 (UPC-1) foi quantificada no tecido adiposo marrom (TAM) e o conteúdo de ANGIO II no TAM, TAB e hipotálamo. As etapas iniciais da sinalização da insulina foram avaliadas por imunoprecipitação e immunoblotting das proteínas envolvidas como o receptor da insulina (IR), substrato 1 e 2 do IR (IRS-1 e IRS-2), enzima fosfatidilinositol 3 quinase (PI-3q), proteína quinase B (Akt/PKB), ativação da proteína c-jun NH2-terminal quinase (JNK) e fosforilação em serina 307 do IRS-1. O PC no desmame foi semelhante entre os grupos de dieta. No entanto, na idade adulta os ratos em dieta HO apresentaram maior PC, adiposidade visceral, glicemia e insulinemia de jejum, concentração de ANGIO II plasmática e aumento do conteúdo de ANGIO II no TAM. Por outro lado, nestes mesmos animais a dieta HO diminuiu o consumo de ração, o gasto energético, a expressão da proteína UCP-1, adiponectina plasmática e o conteúdo de ANGIO II no TAB. A atividade motora não foi diferente entre os grupos estudados. A dieta HO diminuiu a via IR/PI-3q/Akt/Foxo1 de sinalização da insulina no fígado e músculo. Por outro lado, parte desta via (IRS-2/Akt/Foxo1) mostrou-se aumentada no TAB. No fígado e músculo houve um aumento da fosforilação da proteína JNK associada com maior fosforilação do IRS-1ser307 no grupo HO. Em conclusão, a restrição ou sobrecarga crônica de sal altera a evolução ponderal associada com modificações no balanço energético e no perfil hormonal na idade adulta. A resistência à insulina induzida pela dieta HO é tecido-específico e foi acompanhada por uma ativação da proteína JNK e um aumento da fosforilação dos resíduos de serina 307 do IRS-1.<br>Restriction of sodium chloride intake has been associated with insulin resistance (INS-R) and obesity. The molecular mechanisms by which the low salt diet (LSD) can induce INS-R and obesity have not yet been established.The aim of the present study was to evaluate the influences of salt intake on body weight (BW) and on insulin signaling in liver, muscle and white adipose tissue (WAT). Wistar rats were fed a LSD, normal (NSD), or high (HSD) salt diet since weaning. At 12 weeks of age, BW, blood pressure(BP),energy balance, food intake, plasma glucose and angiotesin II (ANGIO II), and hormonal profile were evaluated. Afterward, motor activity, HOMA index, uncoupling protein 1 expression (UCP-1) and tissue adipose ANGIO II content was determined. The early steps of insulin signaling (IR: insulin receptor, IRS-1 and IRS-2: IR substrate 1 and 2, PI-3K: phosphatidylinositol 3-kinase), Akt (protein kinase B) phosphorylation, JNK (c-jun NH2-terminal kinase) activation and IRS-1ser307 (serine 307 of IRS-1) phosphorylation were evaluated by immunoprecipitation and immunoblotting. LSD increased BW, visceral adiposity, blood glucose, insulin, leptin, plasma ANGIO II and its content in BAT. Otherwise, LSD decreased food intake, energy expenditure, UCP-1 expression, adiponectin and ANGIO II content in WAT. Motor activity was not influenced by the dietary salt content. In LSD, a decreasing in IR/PI-3K/Akt/Foxo1 was observed in liver and muscle and an increase in this pathway was showed in adipose tissue. JNK activity and IRS-1ser307 phosphorylation were higher in liver and muscle. In conclusion, LSD induced obesity and insulin resistance due to changes in energy expenditure, SRA and insulin signaling. The INS-R is tissuespecific and is accompanied by JNK activation and IRS-1ser307 phosphorylation.
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Netjes, Robert Bryan. "Relationships between weight, HOMA IR, leptin, adiponectin and interleukin-6, before and after a calorie restricted diet intervention, and in a 6-8 month post diet period, in overweight and obese individuals at risk for type 2 diabetes." Pullman, Wash. : Washington State University, 2008. http://www.dissertations.wsu.edu/Thesis/Fall2008/R_Netjes_120308.pdf.
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Thesis (M.Nurs.)--Washington State University, December 2008.<br>Title from PDF title page (viewed on Mar. 4, 2009). "Intercollegiate College of Nursing." Includes bibliographical references (p. 71-87).
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Grandisoli, Laura Fantazzini. "Influência da intervenção nutricional para perda de peso sobre o perfil cardiometabólico e impacto das adipocitocinas no reganho de peso." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-14122015-125751/.
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Introdução - Nas últimas décadas a prevalência de obesidade aumentou progressivamente em nível global. O tecido adiposo e as adipocitocinas têm papel de destaque em inúmeros processos metabólicos. O desbalanço de adipocitocinas como leptina e adiponectina são comuns em obesos, exercendo efeito relevante nas complicações vasculares e alterações metabólicas comumente observadas entre indivíduos com excesso de peso. As alterações nas concentrações de leptina e adiponectina decorrentes da perda de peso relacionam-se a benefícios no perfil cardiometabólico, porém podem influenciar o reganho de peso. Objetivo - Avaliar a influência da intervenção nutricional para perda de peso sobre o perfil cardiometabólico e o impacto das concentrações de leptina e adiponectina no reganho de peso de indivíduos adultos. Métodos Ensaio clínico não controlado, de séries temporais. Foram incluídos indivíduos de ambos os sexos, com Índice de Massa Corporal (IMC) 25 kg/m2, atendidos no ambulatório de Nutrição do Hospital Universitário da USP. A intervenção durou 4 meses e consistiu em 5 encontros em grupo. Os participantes foram orientados a manter dieta com restrição calórica média de 18 por cento e receberam orientações sobre alimentação saudável, fibras alimentares, leitura de rótulos e alimentos funcionais. Nos momentos basal (T0), ao término da intervenção (T1) e 6 meses após o término (T2) foram avaliados parâmetros bioquímicos, antropométricos, de composição corporal, consumo alimentar, nível de atividade física e pressão arterial. Os resultados foram analisados por Equações de Estimação Generalizadas (GEE), análises de correlação e modelos de regressão linear (nível de significância p<0,05). Resultados Quarenta e três indivíduos participaram do estudo. A perda de peso média foi de 1,0kg (0,96 por cento ) (p=0,029). Vinte e sete indivíduos (62,8 por cento ) perderam peso (-2,37kg, -2,47 por cento ), com redução significativa de todas as variáveis antropométricas. Dentre os que ganharam 7 peso (+1,32kg, +1,58 por cento ), não houve aumento significativo na circunferência da cintura e porcentagem de gordura. Em T1 houve redução significativa das concentrações médias de colesterol total (-9 mg/dL, p=0,004), LDL-C (-7 mg/dL, p=0,017), colesterol não-HDL (-9 mg/dL, p=0,002), CT/HDL-C (-0,2, p=0,004) e LDL-C/HDL-C (-0,2, p=0,008). A análise estratificada segundo ganho e perda de peso evidenciou redução significativa dos mesmos parâmetros, independente de ganho ou perda. Dois terços dos indivíduos que perderam peso apresentaram reganho em T2 (74,9 por cento do peso perdido), fato que impactou diretamente na piora das medidas antropométricas e parâmetros bioquímicos. Em T2, somente as concentrações de LDL-C e colesterol não-HDL mantiveram-se abaixo do basal. Apesar do reganho de peso observado após o término da intervenção, as melhorias na qualidade da dieta apresentadas em T1 permaneceram 6 meses após o término da intervenção. Não houve associação entre as concentrações de leptina e adiponectina e o reganho de peso. Conclusão A intervenção teve influência positiva em importantes fatores de risco cardiometabólico. As concentrações de leptina e adiponectina não permitiram prever o reganho de peso.<br>Introduction Obesity prevalence has increased progressively worldwide in the past decades. Metabolic processes are controlled by substances known as adipokines, produced by the adipose tissue. Obese subjects commonly present a dysfunctional secretory profile of adipokines, leading to metabolic alterations and vascular complications. Weight loss induces changes in leptin and adiponectin levels, which are related to benefits in cardiometabolic profile, but it can also influence weight regain. Objectives To asses the effect of a nutritional weight loss program on overweight and obese adults cardiometabolic profile, and the impact of adipokines in weight regain. Methods Single arm, time series trial. The weight loss program consisted in a 4-month nutritional counselling with 5 group meetings. Topics related to healthy eating, dietary fibre, reading and understanding food labels and functional food were discussed. Subjects received an eating plan with mean caloric restriction of 18 per cent and had biochemical, anthropometric and body composition parameters assessed, as well as blood pressure, physical activity and food consumption. These data were collected before (T0), at the end (T1) and six months after the end of the program (T2), at the University of São Paulos Hospital, Brazil. Results were analyzed using Generalized Estimating Equation (GEE), correlations and linear regression models (p<0.05). Results Forty-three subjects participated in the study. The mean weight loss was 1.0kg (0.96 per cent ) (p=0.029). Twenty-seven subjects (62.8 per cent ) presented a mean weight loss of 2.37kg (2,47 per cent ), and significant reduction of all anthropometric parameters assessed. There were no significant waist circumference and body fat percent increase among subjects who presented weight gain (1.32kg, 1.58 per cent ). At T1, the subjects had significant reduction in mean levels of total cholesterol (-9 mg/dL, p=0,004), LDL-C (-7 mg/dL, p=0,017), non-HDL cholesterol (-9 mg/dL, p=0,002), CT/HDL-C (-0,2, p=0,004) and LDL-C/HDL-C (-0,2, p=0,008). Both groups (which lost and gained weight) had significant reduction of these same parameters, regardless weight gain or loss. Two-thirds of the subjects who lost weight had weight regain at T2 (74,9 per cent of the weight lost), leading to worsening of the anthropometric and biochemical parameters. At T2, only LDL-C and non-HDL cholesterol levels remained below basal levels. Despite weight regain, the improved diet quality observed at T1 remained 6 months afterwards. Leptin and adiponectin levels showed no association with weight regain Conclusion The weight loss program had positive influence on cardiometabolic risk factors. Leptin and adiponectin levels could not predict weight regain.
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Corbalán, Tutau Mª Dolores. "Caracterización de marcadores circadianos de cronodisrupción en obesidad: utilidad en la práctica clínica." Doctoral thesis, Universidad de Murcia, 2013. http://hdl.handle.net/10803/116929.
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Tesis por compendio de publicaciones<br>La gran preocupación que existe actualmente alrededor del peso corporal, está colaborando a la proliferación de innumerables dietas de adelgazamiento entre las personas “no satisfechas con su peso”. En este sentido hemos estudiado la obesidad desde un punto de vista cronobiológico, para poder dilucidar la importancia que tiene la alteración circadiana de ciertos ritmos biológicos en la ganancia de peso o la no pérdida del mismo. El acúmulo de grasa corporal y el grado de lipogénesis en el tejido adiposo podría ser diferente a distintas horas del día, ingiriendo las mismas calorías. A su vez uno de los aspectos más interesantes, es poder conseguir una caracterización cronobiológica de cada individuo, establecer mejoras en las terapias de comportamiento alimentario, introducir nuevos índices que permitan detectar pacientes de riesgo y poder establecer pautas alimentarias y hábitos de vida individualizados que ayuden a estos pacientes a alcanzar la meta de peso propuesta.<br>The great controversy now there about body weight, is collaborating with the proliferation of countless diets among people "not satisfied with their weight." In this sense, we have studied obesity from a chronobiological viewpoint, to elucidate the importance of the alteration of circadian biological rhythms in weight gain or no loss. The accumulation of body fat and the degree of lipogenesis in adipose tissue may be different n accordance with the time of day, even eating the same calories. In turn one of the most interesting aspect, is to be able to characterize the individual chronobiology of each patient, establish improved therapies feeding behavior, introducing new indices to detect patients at risk and to establish dietary patterns and lifestyle habits that help these patients to achieve the proposed weight goal.
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Ferreira, João Marcos Bemfica Barbosa. "Avaliação do metabolismo e atividade inflamatória nas diversas formas evolutivas da doença de Chagas: correlação com disfunção autonômica." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-07022014-144651/.
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INTRODUÇÃO: A cardiopatia chagásica crônica (CCC) apresenta características específicas, tais como: disfunção autonômica e atividade inflamatória exacerbada. Esta fisiopatologia sugere que alguns parâmetros metabólicos podem estar alterados em pacientes chagásicos. O objetivo deste estudo foi avaliar os parâmetros metabólicos e inflamatórios nas diversas formas evolutivas de doença de Chagas e sua correlação com medidas de avaliação do Sistema Nervoso Autônomo (SNA). MÉTODOS: Foram avaliados 60 indivíduos divididos em 4 grupos (n=15): Grupo controle (GC), Grupo FI - forma indeterminada, Grupo ECG- cardiopatia chagásica com alteração eletrocardiográfica sem disfunção ventricular e Grupo IC - cardiopatia chagásica com disfunção ventricular e insuficiência cardíaca. Todos os grupos foram pareados de acordo com sexo, idade e índice de massa corporal. Os pacientes realizaram dosagens sanguíneas de insulina, leptina, adiponectina, interleucina-6 (IL- 6) e fator de necrose tumoral-alfa (TNF-alfa) pelo método de ELISA. O SNA foi avaliado através da variabilidade da frequência cardíaca no holter 24 horas e no teste de inclinação postural. Os valores de RMSSD, pNN50 e do componente alta frequência (AF) foram utilizados como estimativa da atividade parassimpática. Os valores do componente de baixa frequência (BF) estimaram a atividade simpática. A análise estatística foi feita utilizando-se a ANOVA ou teste de Kruskal-Wallis para a comparação entre os grupos, o coeficiente de Spearman para a análise das correlações e a regressão linear múltipla para a análise multivariada. RESULTADOS: A leptina e insulina não apresentaram diferenças significativas entre os grupos [Leptina: GC=3,42 (7,43); FI=3,03 (6,53); ECG=5,56 (6,2); IC=2,86 (2,67) ng/ml; p=0,626. Insulina: GC=3,41 (1,98); FI=4,31 (2,85); ECG=4,30 (3,06); IC=4,58 (2,88) ng/ml; p=0,901] A adiponectina apresentou níveis maiores nos grupos ECG e IC [GC=4766,5 (5529,5); FI= 4003,5 (2482,5); ECG= 8376,5 (8388,5); IC= 8798 (4188) ng/ml; p < 0,001]. IL-6 e TNF-alfa foram maiores no Grupo IC [IL-6: GC=1,85 (6,41); FI=1,58 (1,91); ECG=1,0 (1,57); IC= 31,44 (72,19) pg/ml; p=0,001. TNF-?: GC=22,57 (88,2); FI=19,31 (33,16); ECG=12,45 (3,07); IC=75,15 (278,57) pg/ml; p=0,04]. A insulina, leptina e TNF-alfa não apresentaram correlações significativas com medidas de avaliação do SNA. A adiponectina apresentou correlação positiva com o componente AF (r= 0,336; p= 0,009) e correlação negativa com o componente BF (r= -0,336; p= 0,009). A interleucina-6 apresentou correlação positiva com o componente AF (r= 0,419; p=0,004) e correlação negativa com o componente BF (r= -0,393; p= 0,007). Porém, na análise multivariada apenas a adiponectina apresentou correlação significativa com medidas de função do SNA. CONCLUSÃO: A adiponectina foi maior nos grupos ECG e IC. A IL-6 e o TNF-alfa foram maiores no grupo IC. O aumento dos níveis de adiponectina esteve associado a diminuição da atividade simpática e predomínio da atividade parassimpática.<br>BACKGROUND: Chagas disease (CD) has specific characteristics such as autonomic dysfunction and increased inflammatory activity. This pathophysiology suggests that metabolic parameters can be altered in patients with CD. The aim of this study was to evaluate the metabolic and inflammatory parameters in different forms of CD and their correlation with Autonomic Nervous System (ANS) measures. METHODS: We evaluated 60 subjects divided into 4 groups (n=15): control group (CG), group IF (indeterminate form); group ECG (ECG abnormalities and normal left ventricular function in echocardiogram) and HF group (heart failure with left ventricular dysfunction). All groups were matched for age, sex and body mass index. The patients underwent insulin, adiponectin, leptin, interleukin-6 (IL-6) and tumor necrosis factor-alfa (TNF-alfa) measurements by ELISA. The Autonomic Nervous System was assessed by heart rate variability in 24-hour Holter and tilt test. RMSSD, pNN50 and High Frequency (HF) component values were used to estimate parasympathetic activity and low frequency (LF) components were used to estimate sympathetic activity. Statistical analyses were performed using ANOVA or Kruskal- Wallis tests to compare groups. Spearman coefficient was used for correlation analysis and linear regression for multivariate analysis. RESULTS: No significant differences were observed in leptin and insulin levels between groups. [Leptin: CG=3.42 (7.43); IF=3.03 (6.53); ECG=5.56 (6.2); HF=2.86 (2.67) ng/ml; p=0.626. Insulin: CG=3.41 (1.98); IF=4.31 (2.85); ECG=4.30 (3.06); HF=4.58 (2.88) ng/ml; p=0.901]. Adiponectin was higher in ECG and HF groups. [CG=4766.5 .(5529.5); IF= 4003.5 (2482.5); ECG= 8376.5 (8388.5); HF= 8798 (4188) ng/ml; p < 0.001)]. IL-6 and TNF-alfa were higher in HF group. [IL-6: CG=1.85 (6.41); IF=1.58 (1.91); ECG=1.0 (1.57); HF= 31.44 (72.19) pg/ml; p=0.001. TNF-alfa: CG=22.57 (88.2); IF=19.31 (33.16); ECG=12.45 (3.07); HF=75.15 (278.57) pg/ml; p=0.04]. Insulin, leptin and TNF-alfa did not correlate with autonomic dysfunction. Adiponectin correlated positively with HF component (r=0.336; p= 0.009) and inversely with LF component (r= -0.336; p=0.009). IL-6 correlated positively with HF component (r= 0.419; p=0.004) and inversely with LF component (r= -0.393; p= 0.007). However, in multivariate analysis only adiponectin correlated significantly with ANS measures. CONCLUSION: Adiponectin levels were higher in ECG and HF groups. IL-6 and TNF-alfa were higher in HF group. Higher levels of adiponectin were associated with reduced sympathetic activity and predominance of parasympathetic activity