Thèses : « Tissue Adipokine »

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DeGroat, Ashley. « The Effect of Alcohol Consumption on Adipokine Secretion ». Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3425.

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Alcoholic Fatty Liver Disease (AFLD) is caused by excessive alcohol consumption and is a leading cause of liver related mortalities, with currently no treatments available. The goal of this project was to establish the effect of alcohol consumption on adipose tissue-derived secreted factors, adiponectin and C1q TNF Related Proteins 1-3 (CTRP1-3). We propose that excessive alcohol consumption will reduce circulating levels of adiponectin and CTRPs 1-3. Mice were fed a Lieber-Decarli control or alcohol diet for 10-days with a gavage (NIAAA model) or 6-weeks with no gavage (chronic model). Serum and adipose tissue were collected and CTRPs 1-3 and adiponectin levels were examined by immunoblot analysis. Our results indicate that long-term alcohol consumption effects adipokine secretion in a sex specific manner. Further research will be needed to explore the physiological relevance of these findings, to determine if these changes are beneficial to combat the negative effects of excessive alcohol consumption.

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Magon, Vishakha. « Body Composition and Adipokine Levels in Growth Hormone Antagonist Mice ». Ohio University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1244481356.

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Ahn, Jinsoo. « Roles of Adipose Tissue-Derived Factors in Adipose Tissue Development and Lipid Metabolism ». The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1430496153.

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Ameen, G. I. « Investigating the impact of c-Cbl deficiency in adipose tissue : its role in insulin sensitivity and adipokine production ». Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3028221/.

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Musick, Adam, Madison Shipley, Fei Tu, Chuanfu Li, Valentin Yakubenko et Jonathan Peterson. « Effect of Sepsis on Circulating CTRP3 Levels ». Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/207.

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Effect of Sepsis on Circulating CTRP3 Levels Adam Musick, Madison Shipley, Fei Tu, Chuanfu Li, Valentin Yakubenko, and Jonathan M. Peterson. Adipose tissue is an active endocrine organ which secrets several pro- and anti- inflammatory mediators, collectively called adipokines. Our previous work has identified a novel anti-inflammatory adipokine called C1q TNF Related Protein 3 (CTRP3). Others have previously demonstrated that localized overexpression of CTRP3 protects myocardial tissue from lipopolysaccharide (LPS)-induced sepsis, further supporting the potential protective role of CTRP3. However, endogenous regulation of CTRP3 in response to a sepsis event has not been explored. Further, other adipokines have been identified as diagnostic/prognostic biomarkers for critically ill patients. Therefore, the purpose of this project was to determine the effects of a sepsis event on the circulating CTRP3 levels. METHODS: Gonadal adipose tissue and serum were collected 8 hours after induction of the cecal-puncture and ligation (CLP) model of sepsis or sham control mice. The circulating levels of CTRP3 were quantified by immunoblot analysis. The transcription levels of CTRP3 in adipose tissue were measured by Real-Time PCR. In addition, to explore a potential mechanism for a protective role of CTRP3, thioglycollate-induced peritoneal macrophages were isolated and binding of recombinant CTRP3 was determined by imaging flow cytometry. RESULTS: Circulating CTRP3 levels decreased by approximately 90% compared to sham mice. However, adipose tissue transcription levels of CTRP3 was not difference between CLP and sham mice. Further, imaging flow cytometry demonstrated that CTRP3 binds directly to isolated macrophages. CONCLUSION: The overserved reduction in circulating CTRP3 protein levels and the absence of changes to the CTRP3 transcription, indicate that during sepsis CTRP3 is actively removed from the blood. As CTRP3 binds directly to macrophages and has been previously shown to attenuate LPS-induced macrophage activation these data could indicate that under normal conditions CTRP3 combines with active macrophages to help suppress cytokine overexpression. However, it appears that during sepsis the endogenous CTRP3 levels are quickly depleted. Combine these data support future research to determine if circulating CTRP3 levels are a biomarker indicative of sepsis prognosis and to determine if increasing the circulating levels of CTRP3 could reduce the cytokine storm associated to a sepsis event. Further, as we have demonstrated CTRP3 binds directly to macrophages, future studies are also needed to explore the potential anti-inflammatory mechanism of CTRP3 action on macrophages.

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Zapfe, Luise. « mRNA-Expression von Genen des Fett- und Kohlenhydratstoffwechsels unterschiedlicher Fettlokalisationen bei Kühen ». Doctoral thesis, Universitätsbibliothek Leipzig, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-62426.

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Problemstellung: Die Tiergesundheit hat sich bei Milchkühen in den letzten Jahren weltweit negativ entwickelt. Wichtigster Ausdruck dafür ist die auf ca. 2,4 Jahre verkürzte Nutzungsdauer. Dabei spielt das Fettmobilisationssyndrom eine dominante Rolle. Das Fettgewebe ist nicht nur als reiner Energiespeicher, sondern als endokrines stoffwechselaktives Organ anzusehen. Untersuchungen an Menschen und Mäusen haben gezeigt, dass das Fettgewebe in Abhängigkeit von seiner Lokalisation im Körper unterschiedlich auf metabolische und hormonelle Stimuli reagiert. Es gibt Hinweise, dass auch für das Rind ähnliche Differenzen angenommen werden können. Zielstellung: Um die Eigenschaften des bovinen Fettgewebes und seine Rolle im Energiestoffwechsel besser charakterisieren zu können, war das Ziel der vorliegenden Untersuchung, die mRNA-Expressionen ausgewählter für den Fettstoffwechsel relevante Gene im bovinen Fettgewebe an verschiedenen Lokalisationen grundlegend in gesunden Rindern zu untersuchen. Material und Methoden: Die Probenentnahme erfolgte an 12 gesunden Schlachtkühen direkt nach der Tötung, die aufgrund Schwermelkbarkeit oder Unfruchtbarkeit geschlachtet wurden. Das Fettgewebe wurde aus dem Omentum majus, dem Depotfett der Niere, im kaudalen Beckendrittel (retroperitoneales Fett), dem Hüftbereich (subkutanes Fett) und dem Fett an der Herzbasis entnommen. Die Proben wurden in Flüssigstickstoff tiefgefroren, auf Trockeneis transportiert und bis zur Untersuchung bei -70°C gelagert. Die mRNA-Expression für die verschiedenen Gene (Hormonsensitive Lipase (HSL), Lipoproteinlipase (LPL), Fettsäuresynthase (FASN), Leptin, Adiponektin, Retinolbindungsprotein 4 (RBP4), Tumornekrosefaktor  (TNF) und Interleukin 6 (IL-6), Fettsäurebindungsproteine (FABP3, 4 und 5) und Glukosetransporter 4 (GLUT4)) , wurden mit einer quantitativen real time (RT)-PCR gemessen. Ergebnisse: Die mRNA-Expressionen der verschiedenen oben genannten Gene, ausgenommen IL-6 und FABP3, sind im bovinen Fettgewebe nachweisbar. Die mRNA-Expressionen unterschieden sich in den einzelnen Fettdepots nicht signifikant. Ausnahme hierbei bildete RBP4, dessen mRNA im pericardialen Fett signifikant höher exprimiert war als im subkutanen und omentalen Depot. Die mRNA-Expression des subkutanen, omentalen, perirenalen und pericardialen Fettdepots korrelierten signifikant positive untereinander. Schlussfolgerung: Die mRNA-Expressionen der in den Fettstoffwechsel involvierten und untersuchten Gene gesunder Rinder waren nachweisbar, unterschieden sich jedoch nicht signifikant von einander mit Ausnahme der RBP4 mRNA. Die positiven signifikanten Korrelationen zwischen dem subkutanen, omentalen, perirenalen und pericardialen Fettlokalisationen und gleichmäßigen Expressionen innerhalb der Gewebe deuten auf eine einheitliche Fettmetabolismus des gesamten Körpers. Verglichen mit Ergebnissen der Humanmedizin sind nur wenige Übereinstimmungen (HSL, LPL, GLUT4,TNF) zu eruieren. Weitere Studien mit gesunden Tieren im Vergleich zu erkrankten Rindern müssen klären, ob eine mögliche Verschiebung der mRNA-Konzentrationen auf das Fettmobilisationssyndrom hinweisen
Purpose: Over the last years, the situation of animal health concerning dairy cows has developed worldwide in an adverse way. Most important indicator is the shortened useful life of approx. 2.4 years. The fat mobilization syndrome plays a dominant role in this process. Apparently, fatty tissue does not only serve as a mere energy reservoir, but also as an endocrin organ with metabolic activity. Researches on humans and mice have shown fatty tissue to react on metabolic and hormonal stimuli in different ways, depending on its body localization. There are dues to anticipate, similar differences in cattle. Objectives: In order to better characterize the attributes of bovine fatty tissue and its purpose in metabolism, the present study aims examine basically the expression of mRNA in selected genes which are important for lipid metabolism in bovine fatty tissue of different localizations in healthy cattle. Methods and material: Samples where taken from twelve carcasses of healthy dairy cows slaughtered for reason of difficult milking or infertility directly after killing. Fatty tissue was taken from omentum major, kidney capsula, caudal pelvis area (retroperiteonal fat), hip area (subcutaneous fat), and cardiac base. It was instantly quick-freezed in liquid nitrogen, put on dry ice while transporting, and stored at -70°C until analysis. The expression of mRNA of different genes (hormone-sensitive lipase (HSL), lipoproteine lipase (LPL), fatty acid synthase (FASN), fatty acid binding proteine (FABP3,4 and 5), retinol binding proteine 4 (RBP4), adiponectine, glucose transporter 4 (GLUT4), leptin, interleukin-6 (IL-6), and tumor necrosis factor a (TNFα) was measured by means of a quantitative real-time (RT)-PCR. Results: The mRNA-expressions of all these different genes except IL-6 and FABP3 were detected in bovine fatty tissue. The differences of mRNA-expression between sample localization were not statistically significant. RBP4 was excepted, which mRNA showed a significantly higher expression in pericardial fat than in subcutaneous and omental fat, respectively. The correlation between mRNA-expressions of subcutaneous, omental, pericardial and perirenal fat was significant. Conclusions: The mRNA-expression of examined genes being involved in fatty tissue metabolism, were detected in healthy cattle, but were not significantly different, except RBP4. Significantly positive correlations between subcutaneous, omental, perirenal and pericardial localization and consistent expression indicate an integrative metabolism of the whole body. Compared to results of the human medicine only few analogies (HSL, LPL, GLUT4, TNF) were found. Further studies comparing healthy and diseased cattle will have to prove, if possible displacements of the mRNA-level can indicate the fat mobilization syndrome being present

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Neves, Karla Bianca. « Efeito da adipocina chemerin sobre a reatividade vascular : análise em aortas de rato ». Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/60/60138/tde-27092012-094715/.

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Embora seja na obesidade onde se observa hipertrofia e hiperplasia dos adipócitos e aumento da síntese e liberação de adipocinas, condição associada com resistência à insulina e disfunção endotelial, é de suma importância entender os efeitos biológicos de adipocinas, mais especificamente da adipocina chemerin, em condições não patológicas. Os mecanismos pelos quais as citocinas liberadas pelo tecido adiposo podem interferir na função vascular ainda não estão totalmente esclarecidos. Além disso, praticamente não se conhecem os efeitos da citocina/adipocina chemerin sobre a função vascular. Levando-se em consideração que o receptor para chemerin está presente no músculo liso vascular e no endotélio, este trabalho avaliou a atividade biológica e celular desta adipocina sobre a vasculatura de animais não obesos. Investigou-se os efeitos produzidos por esta citocina na reatividade vascular, bem como os mecanismos pelos quais ela modifica a função vascular em animais não obesos. A hipótese deste trabalho é que chemerin aumenta a reatividade vascular a estímulos constritores de endotelina-1 (ET-1) e fenilefrina (PhE) e diminui a vasodilatação induzida pela acetilcolina (ACh) e nitroprussitao de sódio (NPS). Nossos objetivos específicos incluíram determinar: 1) se chemerin promove alterações na reatividade vascular; 2) se as alterações de reatividade vascular promovidas por chemerin são mediadas por modificações da função das células endoteliais ou células de músculo liso vascular; 3) quais vias de sinalização (foco na via das MAPKs) estão sendo modificadas por chemerin e como elas contribuem para as alterações de reatividade vascular produzidas por esta citocina. Nosso estudo demonstrou que a adipocina chemerin possui atividade biológica e celular em aortas de ratos não obesos. Chemerin aumentou respostas vasculares a estímulos contráteis (ET-1 e PhE), atuando tanto no endotélio quanto diretamente em células do músculo liso vascular. O aumento da resposta a estímulos contráteis à ET-1 e PhE foi mediado pela via MEK-ERK1/2, COX-1 e COX-2 e aumento da expressão dos receptores para ET-1, ETA e ETB. Além disso, esta adipocina diminuiu a vasodilatação induzida pela ACh, por meio do desacoplamento da eNOS e aparente envolvimento de estresse oxidativo, e pelo NPS, através de ação sobre a guanilato ciclase. Nossos estudos poderão contribuir para um melhor entendimento sobre o papel dos fatores liberados pelo tecido adiposo visceral sobre a função vascular e, consequentemente, sobre as alterações vasculares presentes na obesidade e patologias associadas.
Although hypertrophy and hyperplasia of adipocytes as well as increased synthesis and release of adipokines are commonly observed in obesity, a condition associated with insulin resistance and endothelial dysfunction, it is extremely important to understand the biological effects of adipokines, or more specifically of the adipokine chemerin, in non-pathological conditions,. The mechanisms by which cytokines released by the adipose tissue may interfere with vascular function are not yet fully understood. Furthermore, the effects of the cytokine/adipokine chemerin on vascular function are not known. Considering that the chemerin receptor is expressed by vascular smooth muscle and endothelial cells, this study investigated the effects produced by this cytokine in vascular reactivity, as well as the mechanisms by which it modifies vascular function in non-obese animals. Our working hypothesis is that chemerin enhances vascular reactivity to constrictor stimuli, such as endothelin-1(ET-1) and phenylephrine (Phe), and decreases the vasodilation induced by acetylcholine (ACh) and sodium nitroprussiate (SNP). Our specific aims were to determine: 1) whether chemerin induces changes in vascular reactivity, 2) if the alterations of vascular reactivity induced by chemerin are mediated by changes in the function of endothelial cells or vascular smooth muscle cells, 3) which signaling pathways (focus on the MAPKs pathway) are being modified by chemerin and how they contribute to changes in vascular reactivity produced by this cytokine. Our study showed that the adipokine chemerin has biological and cellular activity in aortas from non-obese rats. Chemerin increased vascular responses to contractile stimuli (ET-1 and PhE), producing effects both in the endothelial and vascular smooth muscle cells. The increased contractile responses to ET-1 and PhE were mediated via activation of MEK-ERK1/2, COX-1 and COX-2 and increased expression of the ETA and ETB receptors. Furthermore, this adipokine reduced the vasodilation induced by ACh via eNOS uncoupling and oxidative stress, and by SNP, via effects in the enzyme guanylate cyclase. Our studies may contribute to a better understanding of the role of factors released by the visceral adipose tissue on vascular function and, consequently, on the vascular lesions in obesity and obesity-associated diseases.

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Fazenda, Maria Inês Nunes. « Estudo da relação entre a obesidade e a hipertensão em cães ». Master's thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2010. http://hdl.handle.net/10400.5/3530.

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Dissertação de Mestrado Integrado em Medicina Veterinária
Nos países desenvolvidos, a prevalência do excesso de peso e da obesidade tem vindo a aumentar a uma taxa alarmante, tanto em humanos como na população canina. O termo “epidemia” é já comummente aplicado a esta realidade. Para os Médicos Veterinários, a obesidade é uma das condições patológicas mais simples de diagnosticar, a maioria fazendo-o unicamente através da inspecção visual. Contudo, a subjectividade inerente a esta práctica faz deste um método pouco útil numa perspectiva clínica. Estimar a percentagem de massa gorda é o procedimento mais exacto para um diagnóstico de obesidade. A obesidade não se resume apenas a um estado patológico de excesso de peso. A Organização Mundial da Saúde define a obesidade humana como a acumulação excessiva de gordura no organismo que induz consequências nefastas para a saúde. Tal como nos humanos, os cães são também susceptíveis às múltiplas e variadas consequências na saúde devido à obesidade, entre elas a hipertensão arterial sistémica. Os mecanismos pelos quais a obesidade induz hipertensão não estão completamente esclarecidos, mas são vários os mecanismos propostos que incluem a retenção anormal de sódio, excesso de actividade do sistema nervoso simpático, hiperactivação do sistema renina-angiotensina-aldosterona, alterações vasculares, secreção de factores de estimulação mineralocorticóide e acumulação intra-abdominal de gordura. Em 1994, a descoberta da leptina, um factor de saciedade produzido predominantemente pelo tecido adiposo e essencial no controlo do apetite e do balanço energético, levou a uma reclassificação do tecido adiposo como um órgão endócrino. O termo “adipocina” foi universalmente adoptado para descrever uma proteína que é secretada nos (e sintetizada pelos) adipócitos. Esta pode actuar localmente (efeito autócrino ou parácrino) e sistemicamente (efeito endócrino), influenciando uma variedade de sistemas biológicos. A implicação de diversas adipocinas na modulação de algumas alterações neurohormonais que conduzem ao aumento da pressão arterial sistémica na obesidade, foca a importância do tecido adiposo como órgão endócrino. Foi realizado um estudo clínico com uma amostra de 30 cães, divididos em dois grupos, de acordo com a classificação da condição corporal segundo o modelo do índice de massa corporal canino proposto por Muller et al. (2008): Grupo O – obesos; Grupo EP – excesso de peso. Da medição da pressão arterial, utilizando o método Doppler modelo 811-BL (Parks Medical Electronics), foram registados aumentos na pressão sistólica em cães com excesso de peso e obesidade, com uma frequência de hipertensão de 43,3%.
ABSTRACT - Study of the relation between obesity and systemic arterial hypertension - In developed countries, the prevalence of overweight and obesity has been increasing at an alarming rate, in both humans and canine population. The term “epidemic” is now commonly applied to this reality. For Veterinarians, obesity is one of the pathological conditions easier to be diagnosed, the majority doing so only by visual inspection; however, the subjectivity inherent in this practice makes this a useless method in a clinical perspective. Estimate the percentage of fat mass is the most accurate procedure for a diagnosis of obesity. Obesity is not just a pathological condition of excess weight. The World Health Organization defines human obesity as an excessive accumulation of fat in the body that induces adverse effects on health. As in humans, dogs are also liable to multiple and varied effects on health due to obesity, including systemic arterial hypertension. The mechanisms by which obesity induces hypertension are not completely understood, but there are several proposed mechanisms including abnormal sodium retention, overactivity of the sympathetic nervous system, hyperactivation of the renin-angiotensin-aldosterone system, vascular disorders, secretion of mineralocorticoid-releasing factors and accumulation of intra-abdominal fat mass. In 1994, the discovery of leptin, a satiety factor produced predominantly by adipose tissue and essential in controlling appetite and energy balance, led to the reclassification of adipose tissue as an endocrine organ. The term “adipokine” was universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It can act locally (autocrine or paracrine effect) and systemically (endocrine effect), influencing multiple biological systems. The implication of several adipokines in the modulation of some neurohormonal changes that led to increased systemic blood pressure in obesity focuses the importance of adipose tissue as an endocrine organ. It was conducted a clinical study with a sample of 30 dogs, divided into two groups according to the classification of body condition in the canine body mass index model proposed by Muller et al. (2008): Group O – obese; group EP – overweight. When measuring blood pressure using the Doppler method model 811-BL (Parks Medical Electronics), it has been recorded an increase in blood pressure in overweight and obese dogs, with a hypertension frequency of 43, 3%.

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Axelsson, Jonas. « Fat tissue, adipokines and clinical complications of chronic kidney disease / ». Stockholm : Department of Clinical Science, Intervention and Technology, Divisions of Renal Medicine and Baxter Novum, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-653-0/.

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Riesco, Acevedo David Gerardo. « New adipokines vaspin and omentin, circulating levels, gene expression in adipose tissue and relationship of circulating levels with nonalcoholic fatty liver disease ». Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/379550.

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L'obesitat és una situació d'excés de massa de greix corporal que pot conduir a la síndrome metabòlica (SM). Omentin es produeix i és secretada pel TAV i pot tenir un paper antiinflamatori important en estats pro-inflamatoris. La disminució dels nivells circulants i de l'expressió génica de vaspina s'associa a empitjorament de la diabetis i la pèrdua de pes corporal. Simultàniament a l'augment de la incidència de l'obesitat i la diabetis, augmenta la prevalença de l'hepatopatia grassa no alcohòlica (HGNA). La prova gold standard per al diagnòstic histològic és la biòpsia hepàtica. Atès que és una tècnica invasiva, hi ha un interès en el desenvolupament de biomarcadors no invasius per a la identificació d'esteatohepatitis. Els objectius van ser analitzar els nivells circulants d’omentin i vaspina, la seva expressió gènica en teixit adipós en dones amb obesitat mórbida (OM) enfront de dones amb normopès. Es va examinar la seva associació amb les diferents variables bioquímiques, així com l'ús clínic dels nivells circulants d’omentin i vaspina com a potencials biomarcadors de la presència de HGNA. Primer, es van analitzar els nivells circulants i expressió génica de vaspina i omentina en individus amb pes normal i OM. Després, es van analitzar 40 mostres de fetge de les dones amb OM. Els resultats mostraren disminució dels nivells circulants d’omentin a l'OM, presentant correlació inversa amb els paràmetres glucèmics i amb el SM. L'expressió d’Omentin estava disminuïda en OM. En contrast, els nivells de vaspina en els OM no van ser diferents dels controls, amb una correlació inversa amb els nivells de lipocalina-2 i IL6. L'expressió de vaspina va ser significativament més gran en els OM. Quant a l’HGNA, els resultats van objectivar augment dels nivells circulants d’omentin en els pacients amb EHNA respecte l’esteatosi simple. D'altra banda, el rendiment dels nivells d’omentin per al diagnòstic d’EHNA va mostrar una excel•lent AUROC. Les principals conclusions són que omentin sembla exercir un efecte protector front l'obesitat, mentre que els seus nivells circulants augmenten paradoxalment en els pacients amb EHNA.
La obesidad es una situación de exceso de masa grasa corporal que puede conducir al síndrome metabólico (SM). Omentin se produce y es secretada por el TAV y puede tener un papel antiinflamatorio importante en estados pro-inflamatorios. La disminución de los niveles circulantes y de la expresión génica de vaspina se asocia a empeoramiento de la diabetes y la pérdida de peso corporal. Simultaneamente al aumento de la incidencia de la obesidad y la diabetes, aumenta la prevalencia de la hepatopatía grasa no alcohólica (HGNA). Dado que la biopsia hepática es una técnica invasiva, existe un interés en el desarrollo de biomarcadores no invasivos para la identificación de esteatohepatitis. Los objetivos fueron analizar los niveles circulantes de omentin y vaspina, su expresión génica en el tejido adiposo en mujeres con obesidad mórbida frente a mujeres con peso normal. Se examinó su asociación con las variables bioquímicas así como el uso clínico de los niveles circulantes de omentin y vaspina como potenciales biomarcadores de la presencia de la HGNA. Primero, se analizaron los niveles circulantes y la expresión génica de vaspina y omentin en sujetos con normopeso y obesidad mórbida (OM). Después, se analizaron 40 muestras de hígado de las mujeres con OM. Los resultados mostraron disminución de los niveles de omentin en la OM, presentando correlación inversa con los parámetros glucémicos y el SM. La expresión de Omentin estaba disminuida en la OM. En contraste, los niveles séricos de vaspina en los OM no fueron diferentes de los controles, con una correlación inversa con los niveles de lipocalina-2 e IL6. La expresión de vaspina fue mayor en los OM. En cuanto a la HGNA, demostramos un aumento de los niveles circulantes de omentin en los pacientes con EHNA respecto a aquellos con ES. El rendimiento de los niveles de omentin para el diagnóstico de EHNA mostró una excelente AUROC. Las conclusiones son que omentin parece ejercer un efecto protector frente la obesidad, mientras que sus niveles circulantes aumentan paradójicamente en los pacientes con EHNA.
Obesity is a situacion with excess of body fat mass that can lead to metabolic syndrome. Omentin is produced and secreted by VAT and may have an important anti-inflammatory role in pro-inflammatory states. Decreases in vaspin expression and plasma levels accompany worsening of diabetes and body weight loss. In parallel with increased incidence of obesity and type 2 diabetes, the prevalence of non-alcoholic fatty liver disease (NAFLD) is growing worldwide. Because liver biopsy is an invasive procedure there is strong interest in developing non-invasive biomarkers for identifying steatohepatitis in NAFLD. The main objectives of this doctoral thesis were to analyze omentin and vaspin gene expression in VAT and SAT as well as circulating levels in a group of morbidly obese women versus normal-weight control women and its associations with the clinical-biochemical variables as well as the clinical use of circulating omentin and vaspin levels as biomarkers for the presence of NAFLD. First, we analyzed the circulating levels and gene expression of vaspin and omentin in normal-weight and morbidly obese (MO) subjects. Then, we analyzed 40 liver samples from MO women. We showed lower circulating omentin levels in the MO, correlating inversely with glucidic metabolism parameters and also with MetS. Omentin mRNA expression in VAT was reduced in MO. In contrast, serum vaspin levels in the MO were not significantly different from those in the controls, correlating inversely with lipocalin-2 and interleukin-6 levels. Vaspin mRNA expression was significantly higher in the MO. Regarding NAFLD, we revealed increased circulating omentin levels in NASH patients in comparison with SS. The performance of omentin in diagnosing NASH showed an excellent AUROC. In conclusion, the main findings of this doctoral thesis are that omentin appears to exert a protective effect against obesity, whereas circulating omentin levels are paradoxically increased in patients with NASH.

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Ryan, Vivien Hartley. « Studies on the expression and secretion of adipokines in canine white adipose tissue ». Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502546.

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Obesity is now one of the most common medical disorders of companion animals (dogs, cats and horses) and is defined by the expansion of white adipose tissue mass. This tissue is now known to be major endocrine and secretory organ, releasing different protein hormones and signals termed adipokines. A number of these are linked to inflammation and immunity, and a role for inflammation-related adipokines in the development of obesity-associated diseases in humans is increasingly recognised. The specific aim of this project was to examine the extent to which canine adipose tissue produces various adipokines and to determine some of the factors which regulate their production.

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Amosse, Jérémy. « Etude et caractérisation des vésicules extracellulaires dans un contexte d’obésité Phenotyping of circulating extracellular vesicles (EVs) in obesity identifies large EVs as functional conveyors of Macrophage Migration Inhibitory Factor Extracellular vesicles and cardiovascular disease therapy ». Thesis, Angers, 2019. http://www.theses.fr/2019ANGE0037.

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Les vésicules extracellulaires (VEs) sont des nanovésicules dérivées de la membrane cellulaire reconnues comme des vecteurs de communication intercellulaire participant ainsi à de nombreux processus physiopathologiques. Deux sous-types de VEs peuvent être distingués sur la base de leur origine subcellulaire et leur taille : les grosses vésicules/microvésicules (ou lEVs) et les exosomes (ou sEVs). Dans un contexte d’obésité, les VEs ont été impliquées dans le développement des complications métaboliques, notamment l’insulino-résistance. Une étude plus approfondie reste nécessaire pour identifier les acteurs moléculaires impliqués dans ces mécanismes, dans un but thérapeutique ou pour l’identification des VEs adipeuses à des fins de biomarqueurs. Mon projet de thèse a consisté à caractériser les sous-types de VE adipeuses, à évaluer leur sécrétion et leur proportion dans la circulation sanguine ou encore leurs effets métaboliques respectifs sur des cellules/tissus cibles. Dans un premier temps, nous avons évalué la contribution des VEs circulantes dans le transport des adipokines connus pour participer à la mise en place des dysfonctions métaboliques. Nous montrons qu’une majorité du facteur MIF (Macrophage migration Inhibitory Factor) circule associé aux grosses VEs dans le sang identifiant une nouvelle voie de sécrétion pour cette protéine. MIF associé aux lEVs est fonctionnel et utilise son activité tautomérase pour activer la voie ERK, révélant un mécanisme d’activation de l’inflammation différent de celui utilisé par le MIF soluble. La forme de MIF associée aux VEs pourrait ainsi participer aux effets inflammatoires induits par ce facteur. Dans un second temps, nous souhaitions quantifier la proportion de VEs dérivées du TA se retrouvant dans la circulation sanguine. La caractérisation des VEs sécrétées par les différents dépôts adipeux murins dans un contexte sain et d’obésité a révélé la forte présence d’adiponectine, très enrichie dans les sEVs, sous la forme d’oligomères métaboliquement actifs. Le contenu en adiponectine des VEs est significativement diminué avec l’obésité, à l’image de l’adiponectinémie, et nous révélons une adsorption aspécifique de l’hormone adipocytaire sur la surface des VEs. Sur la base de ces résultats, nous concluons au manque de fiabilité de l’utilisation de l’adiponectine comme marqueur phénotypique des VEs adipocytaires circulantes. Dans une dernière partie, nous avons étudié les effets des sEVs et lEVs dérivées de tissus adipeux (TA) de souris témoins ou obèses sur le métabolisme et le phénotype adipeux de souris. Nos premières expériences confirment la capacité des sEVs obèses à induire une insulinorésistance périphérique chez des souris saines, qui pourrait être liées à une moindre sensibilité à l’insuline des tissus adipeux (TA) inguinaux et musculaires. En outre, nous révélons la capacité de ces VEs à induire la beigisation du TA et à favoriser la fibrose tissulaire. Enfin, nos données révèlent des effets métaboliques différents selon le sous-type de VEs adipeuses étudié qui pourraient être liées à des capacités différentes à moduler l’inflammation tissulaire. Ainsi, les VEs dérivées du TA apparaissent comme de véritables acteurs de la communication intercellulaire participant aux dysfonctions métaboliques liées à l’obésité. Bien que les mécanismes sous-jacents à l’action de ces VEs restent encore à élucider, nos résultats apportent une meilleure caractérisation de ces vésicules et révèlent la nécessité de distinguer les sous-types de VEs qui produisent des effets métaboliques différents
Extracellular vesicles (EVs) are nanovesicles derived from the cell membrane that are recognized as vectors of intercellular communication and thus participate in many physiopathological processes. Two subtypes of EVs can be distinguished according to their subcellular origin and size: large vesicles/microvesicles (or lEVs) and exosomes (or sEVs). In the context of obesity, EVs have been involved in the development of metabolic complications, including insulin resistance. Nonetheless, additionnal studes are still needed to identify the molecular actors involved in these mechanisms, for future therapeutic use or for the identification of fat-derived EVs for biomarker purposes. My thesis project aims to characterize adipose EV subtypes, to evaluate their secretion and proportion in the bloodstream as well as their respective metabolic effects on target cells/tissues. First, we evaluated the contribution of circulating EVs in the transport of adipokines known to participate to the development of obesity- associated metabolic dysfunctions. We demonstrate that the majority of MIF factor (Macrophage migration Inhibitory Factor) circulates within large EVs in the blood, therefore identifying a new secretion pathway for this protein. Large EVs-associated MIF is functional and uses its tautomerase activity to activate the ERK pathway, revealing a different inflammation activation mechanism from that used by soluble MIF. EV-associated MIF could thus contribute to the inflammatory effects induced by this factor. Second, we wanted to quantify the proportion of adipose tissue (AT)-derived EVs in the bloodstream. Through characterization of EVs secreted by murine adipose depots in healthy and obese context, we revealed adiponectin enrichment in sEVS, retrieved under high oligomeric active forms. However, EV-associated adiponectin is significantly decreased with obesity, paralleling adiponectinemia. We moreover reveal non-specific adsorption of this adipocyte hormone on EV surface. Based on these results, we conclude that the use of adiponectin as a phenotypic marker for identifying and quantifying adipocyte-derived EVs in blood samples is unreliable. Finally, we studied the metabolic effects of fat-derived lEVs and sEVs isolated from control or obese mice following their injection in lean mice. Our first experiments confirm the ability of obese fat-derived sEVs to induce peripherical insulin resistance in healthy mice, which may be related to reduced insulin sensitivity in inguinal AT and skeletal muscle. In addition, we reveal the ability of these EV subtype to induce AT beiging in the recipient mice and to promote AT fibrosis. By comparing metabolic effects of the different injected EV subtypes, we highlighted distinct metabolic effects that may be related to their different abilities to modulate AT inflammation. Thus, EVs derived from AT appear to be crucial players of AT intercellular communication with other organs and likely participate to metabolic dysfunctions related to obesity. Although the mechanisms underlying the action of AT-derived EVs remain to be elucidated, our results provide a better characterization of these vesicles and reveal the need to distinguish EV subtypes since their display different metabolic effects in target tissues

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Viviano, Alessandro. « The role of epicardial adipose tissue adipokines in the genesis of postoperative atrial fibrillation ». Thesis, St George's, University of London, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677184.

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Objectives: We aim to explore the Epicardial Adipose Tissue (EAT) proteome to identify its role in the genesis of postoperative atrial fibrillation (AF). Methods: EAT samples were collected in 76 patients with no history of AF undergoing CABG. 50 were incubated in culture medium. Conditioned media representing EAT secretome were harvested and proteins extracted from the remaining tissues. Samples were analysed by two-dimensional difference in-gel electrophoresis (2D-DIGE) and high-performance liquid chromatographytandem mass spectrometry (HPLC-MSIMS). Gene expression analysis was performed on 24 samples (8 AF vs. 16 controls). Findings were validated by Western blotting. Results: 20 secretome samples (10 vs. 10) and 12 EAT extracts (6 vs. 6), divided according to development of postoperative AF, were analysed by proteomics. The proteomics analysis returned 35 differentially expressed protein spots in the secretome and 16 differentially expressed protein spots in the EAT extracts (p 1.2). Gelsolin (GSN) was significantly reduced in AF (p=O.03). Dimethylarginine dimethylaminohydrolase 2 (DDAH2) was upregulated in AF (p=O.04). SBP1 was increased in AF for the secretome and reduced in the EAT extracts. Catalase (CATA) was downregulated in AF. GSN was consistently found to be downregulated in the AF group by three independent techniques. Conclusions. Systemic inflammatory response to cardiac surgery and oxidative stress are known triggers for AF. GSN exerts antinflammatory properties by severing actin filaments. DDAH2 degrades nitric oxide synthase inhibitor ADMA (asymmetric dimethylarginine), known to increase oxidative stress.

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Dusaulcy, Rodolphe. « Les sécrétions du tissu adipeux : rôles de l'autotaxine et recherche de nouvelles adipokines ». Toulouse 3, 2011. http://thesesups.ups-tlse.fr/1588/.

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Parallèlement à sa fonction de stockage, le tissu adipeux est aujourd'hui considéré comme un organe endocrine dont les sécrétions peuvent agir localement, de façon autocrine et paracrine, et/ou à distance sur de nombreux organes. Le sécrétome du tissu adipeux est composé de facteurs lipidiques, les lipokines, et protéiques, les adipokines. Ces facteurs ont des fonctions diverses dans l'organisme notamment sur le métabolisme énergétique, l'inflammation, ou encore la prolifération cellulaire et l'angiogénèse. La première partie du manuscrit porte sur un médiateur lipidique, l'acide lysophosphatidique (LPA), et l'autotaxine (ATX), une lysophospholipase D sécrétée responsable de sa synthèse. L'expression de l'ATX est augmentée dans le tissu adipeux de sujets obèses et insulino-résistants. Le but de cette étude était de préciser le rôle in vivo de l'ATX adipocytaire au cours de l'obésité et ses conséquences sur les taux plasmatiques de LPA. Pour cela nous avons invalidé le gène codant pour l'ATX spécifiquement dans l'adipocyte chez des souris, à l'aide d'une approche transgénique de type Cre/lox. L'invalidation de l'ATX adipocytaire a entrainé une diminution de 38% du LPA plasmatique comparativement à des souris sauvages. Lorsque ces souris sont soumises à un régime obésogène enrichi en graisses, la masse de leur tissu adipeux augmente de façon plus importante comparativement aux souris sauvages. Ce phénotype est associé à une augmentation de l'expression du récepteur nucléaire PPAR? et de certains de ses gènes cibles (ap2, adiponectine, leptine, Glut-1), ainsi qu'à une augmentation de la tolérance au glucose des souris. Ces résultats montrent que l'ATX adipocytaire contribue fortement aux taux plasmatiques de LPA et qu'elle constitue un frein à l'expansion du tissu adipeux en réponse à un régime gras. La deuxième partie du manuscrit porte sur la recherche de nouvelles adipokines impliquées dans des perturbations du métabolisme glucidique et dans l'inflammation. Nous avons mis en évidence une augmentation d'expression des cytokines inflammatoires IL-6 et MCP1 par des myocytes de la lignée C2C12 traités par des milieux conditionnés (MC) d'explants de tissu adipeux. Nous tentons d'identifier le ou les facteurs responsables de ces effets par une approche de fractionnement de l'activité biologique des MC par isoélectrofocalisation, suivie d'une analyse en spectrométrie de masse. Ce travail illustre les rôles importants joués par les sécrétions du tissu adipeux. Nous avons ainsi mis en évidence un exemple d'autorégulation de la masse adipeuse par l'ATX, et proposé une démarche permettant l'identification de nouveaux facteurs biologiquement actifs
In addition to its storage function, adipose tissue is now considered an endocrine organ whose secretions can act locally in an autocrine and paracrine manner, and / or on distant cells in many organs. The secretome of adipose tissue consists of lipid factors, the lipokines, and protein factors, the adipokines. These factors have various functions in the body including energy metabolism, inflammation, or cell proliferation and angiogenesis. The first part of the manuscript deals with a lipid mediator, lysophosphatidic acid (LPA), and autotaxin (ATX), a secreted lysophospholipase D responsible for its synthesis. The expression of ATX is increased in adipose tissue of obese and insulin resistant individuals. The aim of this study was to clarify the role of adipocyte ATX in obesity in vivo and its impact on plasma levels of LPA. For this, we invalidated the ATX coding gene specifically in adipocytes, using a Cre / lox transgenic approach in mice. The invalidation of adipocyte ATX resulted in 38% reduction of plasma LPA compared with wild-type mice. When these mice are fed an obesogenic high fat diet their mass of adipose tissue increases to a greater extent when compared to wild-type mice. This phenotype is associated with an increased expression of nuclear receptor PPAR? (Peroxisome Proliferator-Activated Receptor-?) and some of its target genes (ap2, adiponectin, leptin, Glut-1), as well as with an improved glucose tolerance of the mice. These results show that adipocyte ATX contributes significantly to plasma levels of LPA and that it behaves as a negative regulator of adipose tissue expansion in response to a high fat diet. The second part of the manuscript focuses on finding new adipokines involved in disturbances of glucose metabolism and inflammation. We have demonstrated an increased expression of the inflammatory cytokines IL-6 and MCP1 in the C2C12 myocytes cell line when they are exposed to adipose tissue conditioned media (MC). Ongoing experiments aim to identify the factors responsible for these effects by fractioning the bioactivity of MC using isoelectric focusing followed by mass spectrometry. This work illustrates the important roles played by the secretion of adipose tissue

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Distel, Emilie. « Physiopathologie du tissu adipeux : carrefour du pyruvate dans le métabolisme des acides gras et adipokines ». Paris 5, 2009. http://www.theses.fr/2009PA05T039.

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Le tissu adipeux (TA) est le principal producteur d'acides gras (AG). L'expansion de ce tissu au cours de l'obésité, conduit à une élévation chronique des AG plasmatiques qui induirait une résistance à l'insuline. Dans l'adipocyte, au cours de la lipolyse, une fraction des AG est ré-estérifiée en triglycérides grâce à la glycéronéogenèse. Au cours de ce travail, nous avons montré que les thiazolidinediones et les réxinoïdes, deux classes pharmacologiques utilisés dans le traitement du diabète de type 2, exerceraient leurs effets hypolipidémiants, en partie, via l'activation de la pyruvate déshydrogénase kinase 4. Nous avons montré que cette enzyme permet de favoriser l'entrée du pyruvate, principal substrat de la glycéronéogenèse, dans la voie glycéronéogénique. De plus, nous avons montré que le TA infrapatellaire, situé sous la rotule, pourrait exercer via une sécrétion importante d'interleukine-6 et de son récepteur soluble, des effets délétères sur l'articulation voisine, participant ainsi à la progression de l'arthrose
Adipose tissue (AT) produces fatty acids (FA). AT expansion during obesity leads to a chronic raise in plasmatic FA, thus participating in the developement of insulin resistance. In adipocyte, during lipolysis, some FA are reesterified into triglycerides by the glyceroneogenic pathway. This work showed that thiazolidinediones and rexinoids, two pharmacological compounds used in type 2 diabetes, exert their hypolipidemic effects through the activation of pyruvate dehydrogenase kinase 4. We showed that this enzyme favors the entrance of pyruvate, which is the main substrate of glyceroneogenesis, into the glyceroneogenic pathway. Furthermore, we showed that the infrapatellar fat pad, localized under the rotula, secretes interleukin-6 and its soluble receptor and could contribute to paracrine inflammation and progressive cartilage damage

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Jarrar, Mohammed Hussein. « Comparative profiling of circulatory levels of adipokines and cytokines in patients with various types of non alcoholic fatty liver disease ». Fairfax, VA : George Mason University, 2007. http://hdl.handle.net/1920/2927.

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Thesis (Ph. D.)--George Mason University, 2007.
Title from PDF t.p. (viewed Jan. 18, 2008). Thesis director: Ancha Baranova Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biosciences. Vita: p. 213 Includes bibliographical references (p. 188-212). Also available in print.

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Miraglia, Fernanda. « Avaliação da evolução de citocinas e marcadores inflamatórios em crianças e adolescentes obesos em tratamento clínico ». reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/77216.

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Introdução: A obesidade infanto juvenil é considerada um grave problema de saúde pública nos países desenvolvidos e em desenvolvimento associando-se a fatores de risco cardiovascular incluindo deposição de gordura abdominal, resistência à insulina (RI), dislipidemia e hipertensão. O tecido adiposo não é mais considerado apenas como um regulador de temperatura corporal ou um protetor mecânico, mas um órgão endócrino que libera adipocinas de ação pró- inflamatória, formando um elo entre adiposidade, síndrome metabólica e doenças cardiovasculares e a inflamação é um estado conseqüente à obesidade. O objetivo deste trabalho foi demonstrar a evolução de adipocinas e do PCRus, ao longo de 12 meses, em crianças obesas usuárias do AmO. Metodologia: Foram acompanhadas crianças e adolescentes em tratamento clínico para obesidade ao longo de 12 meses, avaliados quanto à antropometria, pressão arterial, circunferência de cintura, perfil lipídico, glicemia e insulina jejum, IL6, TNF- α, adiponectina e PCRus em 2 momentos: inclusão e após 12 meses de acompanhamento no AmO. Resultados: Foram avaliadas 27 crianças e adolescentes com mediana de idade de 10,3 anos. Os valores médios do escore-z do IMC baixaram no período (p<0,01), o HDL-c aumentou seus níveis neste período (p= 0,025). As medianas das adipocinas não variaram ao longo de 12 meses: IL-6 (p=0,470), TNF- α (p= 0,753) e adiponectina (p=0,943). 45% da amostra aumentaram seus valores de adiponectina, sendo maior este aumento no sexo feminino. O PCRus baixou ao longo do período (inclusão: 1,67mg/L(IQ:0,53-3,99mg/L); 12 meses: 0,97mg/L(IQ:0,18-2,03mg/L), porém sem diferença estatisticamente significativa p=0,083. Conclusão: As crianças e adolescentes em tratamento clínico para obesidade, após um ano de seguimento, não melhoraram seu perfil de adipocinas, mas baixaram seus valores de mediana de PCRus, embora sem diferença estatisticamente significativa.
Introduction: Obesity in children and adolescents is considered a serious public health problem in developed and developing countries and is associated with cardiovascular risk factors including abdominal fat deposition, insulin resistance (IR), dyslipidemia, and hypertension. Adipose tissue is no longer considered only as a regulator of body temperature or shield mechanic, but an endocrine organ that releases pro-inflammatory adipokines action, forming a link between adiposity, metabolic syndrome and cardiovascular diseases and inflammation is a consequence of the obesity. The objective of this study was to demonstrate the evolution of adipokines and hsCRP over 12 months in obese children users of the AmO (Clinic for Obese Children and Adolescents). Methods: Children and adolescents in clinical treatment for obesity were followed for over 12 months and assessed for anthropometry, blood pressure, waist circumference, lipid profile, fasting glucose and insulin, IL6, TNFalpha, adiponectin, and hsCRP at 2 different times: at inclusion and after a 12-month followup in the AmO. Results: A total of 27 children and adolescents with a median age of 10.3 years old were evaluated. Mean values of BMI z-scores decreased in the period (p <0.01) and HDL-C levels increased during this period (p = 0.025). The median adipokines did not change over 12 months: IL-6 (p= 0.470), TNF-α (p= 0.753), and adiponectin (p = 0.943). 45% of the sample had their adiponectin values increased, being this increase higher in females. The hs CRP lowered over the period (inclusion: 1.67 mg/L (IQ:0.53-3.99m/L) and 12 months: 0.97 mg/L (IQ:0.18-2.03mg/L) but not statistically significant p = 0.083. Conclusion: After a one year follow-up period, children and adolescents in clinical treatment for obesity did not improve their adipokine profile, but lowered their median hsCRP values although there was no statistically significant difference.

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Aldoori, Ayat Dhia. « Elucidation of signaling mediators between adipose and neural tissue ». The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1407845819.

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Margaritis, Marios. « Adiponectin as a regulator of vascular redox state in human atherosclerosis ». Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:d0fe8c70-17b2-4462-8961-87f36815f85d.

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Atherosclerotic cardiovascular disease is a leading cause of death worldwide. Dysregulation of vascular redox state plays a crucial role in the atherosclerotic process. Increased production of vascular superoxide (O2Î-) and other reactive oxygen species (ROS) leads to endothelial dysfunction, a key early step in atherogenesis. Adipose tissue is a source of vasoactive, hormone-like molecules which are termed adipokines. One of the most important adipokines is adiponectin. Adiponectin has been shown to have antioxidant, anti-atherosclerotic effects in cell culture studies and animal models. However, its role in human cardiovascular disease has not been extensively investigated. More specifically, its effects on the human vascular wall and the mechanisms regulating its synthesis in adipose tissue have not been studied before in humans. The aim of my thesis is to explore the role of adiponectin in human atherosclerosis. This was achieved through use of the Oxford CABG Bioresource: a well-phenotyped cohort and tissue bank of patients undergoing cardiac surgery. By employing a range of in vivo and ex vivo techniques, I demonstrate for the first time in humans that adiponectin has direct antioxidant effects in the vascular wall, by directly suppressing pro-oxidant vascular enzymes and restoring redox balance. These effects persist in type 2 diabetes, presence of which is linked to reduced circulating adiponectin levels. Indeed, a variety of stimuli affect adiponectin synthesis in human adipose tissue, with brain natriuretic peptide being a major driver of adiponectin synthesis. However, different adipose tissue depots demonstrate diverse responses to stimuli affecting adiponectin synthesis, owing to their functional and morphological differences. Of particular interest is the fact that synthesis of adiponectin in perivascular adipose tissue is driven by the oxidative stress status of the underlying vessel. This observation led me to document for the first time in humans the existence of a reciprocal, two-way interaction between perivascular adipose tissue and the vascular wall: high vascular oxidative stress leads to release of factors with the ability to up-regulate adiponectin expression in perivascular adipose tissue, acting as a local paracrine defence mechanism attempting to restore vascular redox state. My thesis provides proof-of-concept for this novel cross-talk between adipose tissue and the vascular wall. This can have significant impact in designing new therapeutic strategies against atherosclerosis.

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Caron, Audrey. « Role of Adipose-to-Muscle Communication in PCB126-induced Metabolic Defects ». Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37786.

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Despite the importance of muscle in the development of type 2 diabetes, few studies have investigated the effect of polychlorinated biphenyls (PCBs) on muscle energy metabolism. Previous results from our lab suggested that PCB126 exposure induced an indirect negative effect on muscle mitochondrial function. Since PCBs are stored in adipose tissue, we hypothesized that PCB126 alters adipokine secretion which in turn affects muscle metabolism. Objectives. Study the adipose-to-muscle communication in PCB126-induced metabolic defects. Methods. Communication between adipocytes and myotubes was reproduced by exposing C2C12 or mouse primary myotubes to the conditioned medium (CM) of 3T3L1 adipocytes exposed to environmentally relevant PCB126 levels. Results. PCB126 significantly increased adipokine secretion and decreased mitochondrial function, glucose uptake and glycolysis in insulin resistant (IR) but not in insulin sensitive 3T3L1. However, exposure of myotubes to CM of IR 3T3L1 only decreased glucose uptake and insulin sensitivity, without altering myotubes glycolysis or mitochondrial function. Conclusion. Our results suggest that the increased adipokine secretion by adipocytes could explain the decreased muscle glucose uptake and insulin sensitivity when exposed to PCB126.

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Taube, Annika [Verfasser], Jürgen [Akademischer Betreuer] Eckel et Eckhard [Akademischer Betreuer] Lammert. « Role of Adipokines in the Crosstalk Between Human Adipose Tissue and Skeletal Muscle Cells / Annika Taube. Gutachter : Jürgen Eckel ; Eckhard Lammert ». Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2011. http://d-nb.info/1017593051/34.

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Lubbers, Ellen MR. « Investigation of adiponectin and its receptors in mouse-models of altered growth hormone action : Attempts to understand the link between adipose tissue and longevity ». Ohio University Honors Tutorial College / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1340185494.

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Đorđe, Popović. « Značaj adiponektina u proceni kardiometaboličkog profila i rizika za razvoj tipa 2 šećerne bolesti kod gojaznih osoba ». Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2016. http://www.cris.uns.ac.rs/record.jsf?recordId=101774&source=NDLTD&language=en.

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Gojaznost se najčešće definiše kao uvećanje udela masne mase u ukupnoj telesnoj masi. Danas gojaznost poprima pandemijske razmere i karakter globalnog zdravstveno-socijalnog problema jer predstavlja faktor rizika za razvoj masovnih nezaraznih bolesti, pre svega tipa 2 šećerne bolesti (T2DM) i kardiovaskularnih bolesti. Adipokini su molekule koje luči masno tkivo i koji imaju značajnu ulogu u regulaciji mnogobrojnih procesa u ljudskom organizmu. Adiponektin (ADN) je adipokin sa antidijabetogenim, antiinflamatornim i antiaterogenim dejstvom. Tokom razvoja, pre svega, centralnog tipa gojaznosti dolazi do poremećaja u sekretornom profilu masnog tkiva, nastaje pad serumske koncentracije ADN i dolazi do razvoja mnogobrojnih kardiometaboličkih poremećaja. Cilj rada je ispitivanje značaja određivanja serumskog ADN u proceni kardiometaboličkog profila i utvrđivanje povezanosti njegovog nivoa sa procenjenim desetogodišnjim rizikom za razvoj T2DM kod gojaznih osoba. Studija preseka sprovedena na Klinici za endokrinologiju, dijabetes i bolesti metabolizma, Kliničkog centra Vojvodine je obuhvatila 65 ispitanika sa hiperalimentacionim tipom gojaznosti. Kod ispitanika je procenjen desetogodišnji rizik za razvoj T2DM i sprovedena su odgovarajuća antropometrijska, laboratorijska i morfološka ispitivanja. Ispitanici sa sniženim serumskim ADN su imali nepovoljniji kardiometabolički profil u odnosu na ispitanike sa normalnom vrednošću serumskog ADN dok nije bilo razlike u nivou desetogodišnjeg rizika za razvoj T2DM između navedenih grupa. Takođe, ispitanici sa metaboličkim sindromom (MS) i ispitanici sa nealkoholnom masnom bolešću jetre (NAFLD) su imali niži serumski ADN u odnosu na osobe bez MS i osobe bez NAFLD. Kod gojaznih osoba postoji značajna povezanost serumskog ADN sa većim brojem pokazatelja kardometaboličkog profila ali ne i sa procenjenim desetogodišnjim rizikom za razvoj T2DM.
Obesity is often defined as the significant increase in proportion of fat mass in total body mass. Nowadays, obesity exhibits pandemic proportions and acquires character of the global health and social problem, as it represents the risk factor for the development of non-communicable diseases, especially type 2 diabetes mellitus (T2DM) and cardiovascular diseases. Adipokines are molecules secreted by adipose tissue which play an important role in the regulation of various processes in the human organism. Adiponectin (ADN) is an adipokine with anti-diabetic, anti-inflammatory and anti-atherogenic effects. During development of, above all, central obesity, disorders in the secretory profile of adipose tissue are arising, decline in serum concentrations of ADN advents, which leads to occurrence of numerous cardiometabolic disorders. The aim of study is to examine the significance of determining serum ADN in assessing the cardiometabolic profile, and determining its association with the estimated ten-year risk of developing T2DM in obese persons. Cross-sectional study conducted at the Clinic for Endocrinology, Diabetes and Metabolic Disorders, Clinical Center of Vojvodina, included 65 persons with hyperalimentation type of obesity. Ten-year risk of developing T2DM was assessed and appropriate anthropometric, laboratory and morphological evaluations were performed. Persons with lower serum ADN had worse cardiometabolic profile compared to those with normal serum ADN value, while there was no difference in the level of ten-year risk of developing T2DM between two groups. Also, subjects with metabolic syndrome (MS) and subjects with nonalcoholic fatty liver disease (NAFLD) had lower serum ADN compared to persons without MS and to those without NAFLD. There is a significant association of serum ADN with a larger number of cardiometabolic profile indicators but not with the estimated ten-year risk of developing T2DM.

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Nakamitsu, Patrícia Fernandes Zanotti 1989. « Talidomida controla as alterações inflamatórias e modifica o remodelamento do tecido adiposo durante a obesidade = Thalidomide controls the inflammatory changes and modifies the remodeling of adipose tissue during obesity ». [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312766.

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Orientador: José Predrazzoli Júnior
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T14:31:33Z (GMT). No. of bitstreams: 1 Nakamitsu_PatriciaFernandesZanotti_M.pdf: 13932642 bytes, checksum: 5c0fce47b8f53f69fc7e1bb4ae8609e6 (MD5) Previous issue date: 2014
Resumo: A expansão do tecido adiposo durante a obesidade é dependente de proliferação e maturação de adipócitos, formação de novos vasos sanguíneos, e remodelamento da matriz, e é acompanhada por infiltração de macrófagos e modificações significativas na produção de adipocinas. Estas alterações contribuem para o estabelecimento da inflamação crônica sistêmica de baixo grau. Os agentes imunossupressores são capazes de modular a atividade do sistema imunológico e que podem controlar a resposta inflamatória associada ao tecido adiposo durante a obesidade. Neste trabalho, foi investigada a ação de um fármaco, a talidomida, que possui atividade anti-inflamatória, pró apoptótica, antiproliferativa e antiangiogênica, nas alterações do tecido adiposo induzidas por dieta hiperlipídica. Em camundongos obesos, a administração de talidomida (100 mg/kg/ por 10 dias) reduz a adiposidade, o tamanho dos adipócitos, a ativação da JNK, a produção de TNF-? e leptina, e a infiltração de macrófagos. Em paralelo, aumenta a produção de IL-1ra. A redução da adiposidade parece estar relacionada com a atividade antiangiogênica da talidomida através da inibição de VEGF e TIMP e, a indução de apoptose. In vitro, observou-se inibição de TNF- ? e MCP-1 liberadas por células 3T3-L1 induzida por LPS. Os nossos resultados sugerem que o desenvolvimento de fármacos que são capazes de modular o estado inflamatório e adicionalmente controlar a expansão do tecido adiposo pode ser uma abordagem interessante no tratamento da obesidade
Abstract: Adipose tissue expansion during obesity is dependent on adipocyte proliferation and maturation, angiogenesis and matrix remodeling, and it is followed by a significant macrophage infiltration and adipokine production alterations. These alterations contribute to the establishment of a chronic low grade systemic inflammation. Immunosuppressant agents are able to modify the immune system activity and they can control the inflammatory response associated to adipose tissue during obesity. We investigated the action of a drug, thalidomide, which contains anti-inflammatory, pro-apoptotic, anti-proliferative and anti-angiogenic activities, on adipose tissue alterations induced by a high-fat diet. In obese mice, thalidomide administration (100 mg.kg-10 days) induces a reduction in adiposity, adipocyte size, JNK activation, TNF-? and leptin production, and macrophage infiltration. Aditionally, increases IL-1ra production. Adiposity reduction seems to be related to thalidomide anti-angiogenic activity through VEGF and TIMP inhibition and, apoptosis induction. In vitro, it was observed an inhibition of basal TNF-? and LPS-induced MCP-1 released by 3T3-L1. Our results suggested that the development of drugs that can modulate the inflammatory status and additionally control the expansion of adipose tissue could be an interesting approach in the management of obesity
Mestrado
Farmacologia
Mestra em Farmacologia

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Smith, Jessica. « Adipose tissue secreted factors in specific populations and metabolic states : Implications for energy balance and metabolic health ». Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27012/27012.pdf.

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Famulla, Susanne [Verfasser], Jürgen [Akademischer Betreuer] Eckel et Lutz [Akademischer Betreuer] Schmitt. « Adipose tissue secretion and inflammation - Characterization of novel adipokines and the impact of hypoxia on adipocyte function / Susanne Famulla. Gutachter : Jürgen Eckel ; Lutz Schmitt ». Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2012. http://d-nb.info/1023946998/34.

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Kim, Min Ji. « Altérations des adipokines et de la fonction mitochondriale du tissu adipeux des patients VIH+ lipodystrophiques sous antirétroviraux et des patients obèses ». Paris 6, 2007. http://www.theses.fr/2007PA066034.

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L’obésité et le syndrome lipodystrophique (LD) secondaire au traitement antirétroviral se caractérisent par des perturbations des fonctions adipocytaires contribuant au développement d’une inflammation de bas grade du tissu adipeux (TA). Nous avons étudié, au cours d’un régime de 3 semaines, les variations du système adiponectine dans le TA sous-cutané (TASC) des sujets obèses. L’amélioration de la sensibilité à l’insuline observée chez les sujets intolérants au glucose pourrait s’expliquer par une augmentation d’expression d’un des récepteurs AdipoR1, ce qui pourrait constituer une régulation aiguë du système adiponectine dans le TASC. Nous avons aussi étudié les mécanismes impliqués dans la toxicité mitochondriale chez les patients VIH+ LD. La déplétion en ADNmt dans le TASC des patients était compensée par une prolifération mitochondriale. Elle n’est pas due à une activation transcriptionnelle des principaux facteurs de la biogenèse mitochondriale mais s’accompagne d’une augmentation d’un stress « mitochondrial » et d’une apoptose cellulaire. Enfin, nous avons observé une amélioration des marqueurs moléculaires de l’adipogenèse, de la fonction mitochondriale et de l’inflammation du TA chez des patients VIH+ après 6 mois d’arrêt de traitement. Ces changements favorables sont liés à l’arrêt des analogues de thymidine et des inhibiteurs de la protéase. Ces résultats justifient les stratégies de remplacement des molécules les plus délétères, afin d’obtenir une amélioration de la lipodystrophie voire d’éviter son développement.

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Eva, Klimcakova. « Regulation of human adipose tissue gene expression in relation to obesity and insulin resistance ». Toulouse 3, 2007. http://thesesups.ups-tlse.fr/40/.

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Parmi les mécanismes possibles de l'insulinorésistance associée à l'obésité figurent une altération de la production d'adipokines par le tissu adipeux (TA). Dans une première partie, nous avons étudié des patients obèses soumis à des programmes nutritionnels ou d'activité physique. Les données phénotypiques ont été reliées à l'expression de gènes du TA potentiellement impliqués dans la sensibilité à l'insuline. Nous avons confirmé qu'un entraînement en condition aérobie ou en force améliorait la sensibilité à l'insuline et démontré que ces interventions ne modifiaient pas l'expression génique dans le TA sous-cutané ou les niveaux plasmatiques d'adiponectine, d'interleukine 6, d'interleukine 1 beta et de tumor necrosis factor alpha mais diminuaient les concentrations circulantes de leptine. Différentes phases d'un programme de perte de poids améliorent la sensibilité à l'insuline et diminuent transitoirement les concentrations plasmatiques de la protéine de liaison du rétinol RBP4. Les niveaux d'ARNm ne sont diminués qu'après la première phase à très basses calories. Nos résultats montrent que les adipokines, excepté peut-être la leptine, ne semblent pas des médiateurs des changements d'insulinosensibilité induits par une intervention diététique ou l'exercice physique. Dans une seconde partie, nous avons exploré le rôle des PPARs (peroxysome proliferator-activated receptors) sur la sécrétion de protéines par le TA sous-cutané humain. Il apparaît que les PPARs régulent la production de facteurs sécrétés provenant de différents types cellulaires du TA. Cet ensemble d'études contribuent à notre compréhension des relations entre adipokines et sensibilité à l'insuline
Obesity is associated with insulin resistance (IR) and type 2 diabetes mellitus. Among possible mechanisms leading to IR are increased plasma levels of free fatty acids and altered levels of adipokines secreted from adipose tissue (AT). In the first part of the work, we studied obese patients during different nutritional and physical activity interventions. Phenotypic data were related to the expression of AT genes potentially involved in the regulation of insulin sensitivity (IS) and/or low-grade inflammation. We confirmed that aerobic and dynamic strength training improved IS and demonstrated that these interventions do not promote changes in subcutaneous AT gene expression or in plasma levels of adiponectin, interleukin-6, interleukin-1 beta and tumor necrosis factor-alpha, but decrease circulating leptin level. Very low calorie diet followed by low calorie diet and weight maintenance period enhanced IS in obese women and diminished retinol-binding protein 4 (RBP4) in plasma, but RBP4 mRNA levels were reduced only after very low calorie diet. Our findings indicate that the investigated adipokines, except potentially leptin, might not be mediators of changes in IS induced by lifestyle interventions. In the second part of the work, we investigated the role of peroxisome proliferator-activated receptors (PPARs) on the protein secretion by human subcutaneous AT. .

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Fisette, Alexandre, et Alexandre Fisette. « Implications de la résistine et de la protéine stimulant l'acylation dans le développement de co-morbidités de l'obésité ». Master's thesis, Université Laval, 2010. http://hdl.handle.net/20.500.11794/21370.

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Tableau d’honneur de la Faculté des études supérieures et postdoctorales, 2009-2010
Tableau d’honneur de la Faculté des études supérieures et postdoctorales, 2009-2010
Le tissu adipeux, autrefois perçu comme un organe inerte voué au stockage de gras est maintenant reconnu comme un organe sécrétant de nombreux facteurs, nommés adipokines. Certains de ces facteurs – on en compte plusieurs dizaines – influencent le métabolisme de la même façon que des hormones plus connues comme l’insuline ou le glucagon peuvent le faire. Ce mémoire porte sur l’étude de deux adipokines en particulier, la protéine stimulant l’acylation (ASP) et la résistine, en relation avec l’obésité et ses co-morbidités. Le premier projet visait à étudier les adaptions du métabolisme hépatique dans des modèles murins ne possédant pas de voie de signalisation fonctionnelle de l’ASP, des modèles résistants à l’obésité. Cette étude a permis de démontrer l’absence de stéatose hépatique et de surproduction de lipoprotéines chez ces souris en plus de mettre en évidence une utilisation altérée des substrats énergétiques par le foie. Le second projet visait à étudier les corrélations entre la résistine plasmatique et de nombreux paramètres liés au syndrome métabolique dans une population d’enfants et d’adolescents chinois. Cette étude a démontré que la résistine n’y est pas corrélée avec la résistance à l’insuline, mais qu’elle y est retrouvée en plus grande concentration s’il y a présence d’obésité centrale. Globalement, ce mémoire met en lumière tant de façon fondamentale que clinique les implications physiologiques des deux adipokines étudiées – l’ASP et la résistine – et clarifie leur potentiel thérapeutique.
Le tissu adipeux, autrefois perçu comme un organe inerte voué au stockage de gras est maintenant reconnu comme un organe sécrétant de nombreux facteurs, nommés adipokines. Certains de ces facteurs – on en compte plusieurs dizaines – influencent le métabolisme de la même façon que des hormones plus connues comme l’insuline ou le glucagon peuvent le faire. Ce mémoire porte sur l’étude de deux adipokines en particulier, la protéine stimulant l’acylation (ASP) et la résistine, en relation avec l’obésité et ses co-morbidités. Le premier projet visait à étudier les adaptions du métabolisme hépatique dans des modèles murins ne possédant pas de voie de signalisation fonctionnelle de l’ASP, des modèles résistants à l’obésité. Cette étude a permis de démontrer l’absence de stéatose hépatique et de surproduction de lipoprotéines chez ces souris en plus de mettre en évidence une utilisation altérée des substrats énergétiques par le foie. Le second projet visait à étudier les corrélations entre la résistine plasmatique et de nombreux paramètres liés au syndrome métabolique dans une population d’enfants et d’adolescents chinois. Cette étude a démontré que la résistine n’y est pas corrélée avec la résistance à l’insuline, mais qu’elle y est retrouvée en plus grande concentration s’il y a présence d’obésité centrale. Globalement, ce mémoire met en lumière tant de façon fondamentale que clinique les implications physiologiques des deux adipokines étudiées – l’ASP et la résistine – et clarifie leur potentiel thérapeutique.
Adipose tissue has been recently recognized to function as an endocrine organ in addition to its fat storage capacities. Adipose tissue secretes a number of factors named adipokines. Some of these hormones influence metabolism similarly to other well-known factors such as insulin and glucagon. This thesis is the result of studies done on two particular adipokines, acylation stimulating protein (ASP) and resistin, as well as their relationship with obesity and its co-morbidities. The aim of the first project was to understand the adaptations of hepatic metabolism in murine models with ASP-C5L2 pathway deficiencies, models that are also obesity resistant. This study demonstrated the absence of hepatic steatosis or lipoprotein overproduction in these mice in addition to showing signs of altered substrate use by the liver. The second study evaluated correlations between plasma resistin and several parameters related to the metabolic syndrome in a population of Chinese children and adolescents. This study demonstrated that resistin does not correlate with insulin resistance, but that circulating levels of resistin are increased in the presence of central obesity. Globally, this thesis shows, from both a clinical and basic science perspective, the physiological implications of the two adipokines studied – ASP and resistin – and clarifies their therapeutical potential.
Adipose tissue has been recently recognized to function as an endocrine organ in addition to its fat storage capacities. Adipose tissue secretes a number of factors named adipokines. Some of these hormones influence metabolism similarly to other well-known factors such as insulin and glucagon. This thesis is the result of studies done on two particular adipokines, acylation stimulating protein (ASP) and resistin, as well as their relationship with obesity and its co-morbidities. The aim of the first project was to understand the adaptations of hepatic metabolism in murine models with ASP-C5L2 pathway deficiencies, models that are also obesity resistant. This study demonstrated the absence of hepatic steatosis or lipoprotein overproduction in these mice in addition to showing signs of altered substrate use by the liver. The second study evaluated correlations between plasma resistin and several parameters related to the metabolic syndrome in a population of Chinese children and adolescents. This study demonstrated that resistin does not correlate with insulin resistance, but that circulating levels of resistin are increased in the presence of central obesity. Globally, this thesis shows, from both a clinical and basic science perspective, the physiological implications of the two adipokines studied – ASP and resistin – and clarifies their therapeutical potential.

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Ljung, Lotta. « Aspects on inflammation and cardiovascular comorbidity in rheumatoid arthritis ». Doctoral thesis, Umeå universitet, Reumatologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-57702.

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There is an increased risk for cardiovascular (CV) comorbidity among patients with rheumatoid arthritis (RA), with premature atherosclerosis, and a higher incidence of CV events, compared with the general population. Disease related factors add to the CV risk, and interact with the traditional CV risk factors. The underlying mechanism for this is not completely understood. In active RA there is a loss of muscle mass and an increase in body fat content. Production of cytokines, i.e., adipokines, in the adipose tissue could link the inflammation with the CV system. Control of the inflammation has been suggested to modify the CV risk in RA, and the recently introduced biological drugs, such as the tumor necrosis factor inhibitors (TNFi), have opened up new treatment opportunities. The aim of this thesis was to evaluate aspects of the interaction between inflammation and CV comorbidity in RA using biochemical and epidemiological methods. Methods In the first two studies, patients with established RA were examined for clinical disease activity, and blood samples were analysed for cytokines and adipokines using ELISAs and multiplex technology. In Study I (n RA=23) anthropometric measurements were assessed and in Study II (n RA=51) measurements of intima-media thickness (IMT), and endothelial function (FMD). From a subgroup of patients (Study II, n RA=13) samples of abdominal subcutaneous adipose tissue (SAT) were analysed for content of adipokines. In study III and IV associations between treatment with TNFi and acute coronary syndromes (ACS) were analysed using data from the Swedish Rheumatology Register; in Study III regarding early RA (n TNFi exposed=1,271, n bionaïve RA=4,729), and in Study IV comprising patients with RA of all stages (n TNFi exposed=7,213, n bionaïve RA=17,769) and with a matched general population comparator cohort (n=32,161). Associations between response to TNFi therapy and risk for ACS in the early RA cohort were evaluated in a nested case-control design (cases n=24, controls n=81). Results Serum levels of the cytokines/adipokines interleukin-1 receptor antagonist (IL-1Ra), IL-6, osteopontin, visfatin and TNF were increased in patients compared with controls (p≤0.001-0.036). The amount of TNF receptor II extracted from SAT was greater in patients (p=0.006). The serum (s-) levels of IL-1Ra correlated with s-leptin (r=0.71, p≤0.001) and s-haptoglobin in RA patients (r=0.56, p≤0.01). The result from a factor analysis indicated IL-1Ra to be associated with both adipose tissue and inflammation. Levels of s-visfatin (p=0.019) and s-IL-1Ra (p=0.023), respectively, were positively associated with IMT independently of inflammatory activity and CV risk factors. PAI-1 and MCP-1 extracted from SAT showed inverse associations with IMT. Patients with RA, whether exposed to TNFi or bio-naïve, had a doubled risk for ACS compared with the general population; HR 2.09 (95%CI 1.58-2.76) and 1.80 (1.49-2.17), respectively. No significant associations between risk for ACS and TNFi exposure were detected after adjustments; HR 0.80 (0.52-1.24) in early RA and HR 1.08 (0.82-1.41) in RA of any duration. Furthermore, no association between the risk for ACS and response to TNFi treatment in patients with early RA was observed, OR 1.5 (0.3-6.9). Conclusions The results indicate that cytokines/adipokines may have a role in the development of atherosclerosis in RA patients. A continuing increase in the risk of ACS in RA compared with the general population, despite modern therapeutic strategies, was noted. Neither exposure nor response to treatment with TNFi was associated with any modification of the risk for ACS.

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Ben, Amara Nisserine. « Evaluation du statut en micronutriments lipophiles au cours de l'obésité : relation avec l'inflammation et l'insulino-résistance ». Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5053.

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L’obésité s’accompagne d’un état inflammatoire chronique qui joue un rôle délétère.Cet état associé à l’obésité été impliqué dans le développement de complications métaboliques:insulino-résistance et DT2.Chez les obèses,le TA est un site de production de médiateurs pro et/ou anti-inflammatoires, des adipokines.Les modifications et changements de style de vie et les approches thérapeutiques sont privilégiés pour lutter contre l’obésité.Toutefois,les approches préventives ne doivent pas être négligées,des études épidémiologiques ont mises en évidence une corrélation entre obésité et carence en micronutriments.Par ailleurs,il existe une corrélation inverse entre micronutriments lipophiles et caroténoïdes et la prévalence de l’obésité et du DT2.Le but de cette thèse est de comprendre le lien qui existe entre carence en micronutriments,obésité et complications associés.Une étude clinique transversale a été réalisée chez des obèses non diabétiques.Les résultats nous ont permis de montrer qu’il existe une association positive entre b-carotène et sensibilité à l'insuline chez l'obèse,effet pouvant être lié à une modulation de l'expression de certaines adipokines dont l'adiponectine qui est indépendamment associée à la concentration plasmatique en b-carotène.Une étude préclinique a été menée, dont l'objectif évaluer l'impact de la teneur en vitamines alimentaires sur la prise de poids et l'insulino-sensibilité.Des souris ont été soumises à un régime hypovitaminé.A 10 semaines,ce régime favorise la prise de masse grasse,modifie la sensibilité à l'insuline,en agissant au niveau du métabolisme lipidique hépatique,via une diminution des capacités oxydatives
Obesity is associated with chronic inflammatory condition that plays a deleterious role.This inflammatory state associated with obesity was involved in the development of metabolic complications : insulin resistance and T2DM.Obese, AT is a site for the production of pro and/or anti-inflammatory adipokines, and plays a major role in the development of chronic inflammation associated with obesity.Modifications and changes in lifestyle and therapeutic approaches are preferred to deal with obesity. However,preventive approaches should not be ignored,several epidemiological studies have shown a correlation between obesity and micronutrient deficiency.In addition,there is an inverse correlation between lipophilic micronutrients and carotenoids and the prevalence of obesity and T2DM.The purpose of this thesis is to understand the possible link between LM and carotenoids deficiency, obesity and associated physiological disorders.A cross-sectional study was performed in non-diabetic obese patients.The results allowed us to conclude the existence of a favorable effect of b-carotene on insulin sensitivity in obese patients.This effect may be related to modulation of inflammation or the expression of some adipokines(such as adiponectin), either directly or through its pro-vitamin A activity.A preclinical study was performed; the objective is to assess the impact of the vitamins on weight gain and insulin sensitivity.Mice were subjected to a hypovitaminic diet.After 10 weeks of regimen, we observed an increased adiposity and an altered insulin sensibility.This diet probably acts on the hepatic lipid metabolism via a decrease in oxidative capacity

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Mellouk, Namya. « Etude de trois adipocytokines, adiponectine, visfatine et chémérine au niveau plasmatique et dans plusieurs tissus métaboliques et reproducteurs de différentes espèces ». Thesis, Tours, 2018. http://www.theses.fr/2018TOUR4007.

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Ces travaux de thèse sont focalisés sur l’étude de trois adipocytokines (adiponectine, visfatine et chémérine) chez des espèces dont les anomalies du métabolisme énergétique sont associées à des désordres de la fonction de reproduction. Nos résultats montrent des effets du régime alimentaire sur le métabolisme lipidique et glucidique et de manière moins prononcée sur les fonctions de reproduction chez la vache laitière et la poule reproductrice de souche chair. Ces effets ont en partie été associés aux profils d’expression de l’adiponectine, la visfatine et la chémérine. De plus, nous avons mis en évidence une surexpression du système chémérine/CMKLR1 dans le liquide folliculaire et dans les cellules ovariennes de patientes atteintes du syndrome des ovaires polykystiques associé ou non à une obésité. D’une part, ces découvertes révèlent la possibilité de considérer ces adipocytokines comme de potentiels biomarqueurs de l’évaluation de la croissance, de l’état d’engraissement et de fertilité dans les élevages agricoles. D’autre part, elles suggèrent une potentielle implication de la chémérine dans la régulation des fonctions ovariennes chez la femme
This thesis is focused on the study of three adipokines (adiponectin, visfatin and chemerin) in species that develop abnormalities of energy metabolism associated with reproductive disorders. Our results have shown some diet effects on the lipid and carbohydrate metabolisms and in a less extend, on the reproductive functions in dairy cows and broiler hens. These effects were partly associated with the expression profiles of adiponectin, visfatin and chemerin. In addition, we have demonstrated overexpression of the chemerin/CMKLR1 system in follicular fluid and in ovarian cells of patients with polycystic ovarian syndrome, with or without obesity. First, these findings reveal the possibility of considering these adipokines as potential biomarkers for evaluating growth, fattening status and fertility in agricultural farms. On the other hand, they suggest a potential involvement of chemerin in the regulation of ovarian functions in women

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Cartier, Amélie. « Étude de facteurs impliqués dans la variation de marqueurs inflammatoires présents dans un contexte d'obésité abdominale et de complications métaboliques associées ». Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27063/27063.pdf.

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Dirat, Béatrice. « Les adipocytes associés au cancer : nouveaux acteurs de la progression tumorale : un lien entre obésité et cancer ». Toulouse 3, 2010. http://thesesups.ups-tlse.fr/937/.

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La progression tumorale a été récemment reconnue comme étant le produit d'une interaction dynamique entre les cellules tumorales et leur microenvironnement. Parmi les cellules qui constituent le microenvironnement, les adipocytes sont celles dont le rôle a été le moins bien caractérisé, malgré le fait que les adipocytes représentent le composant cellulaire majoritaire du microenvironnement de certaines tumeurs, comme par exemple le cancer du sein, ou le cancer invasif de la prostate. L'identification du rôle des adipocytes dans la progression tumorale a toute son importance car il a été démontré dans des études épidémiologiques que l'obésité est un facteur de mauvais pronostic dans de nombreux cancers. En effet comme le montre les résultats d'une vaste étude menée à l'institut Curie, les patientes atteintes de cancer du sein, et qui de surcroit sont obèses, présentent des tumeurs plus agressives définies par un stade plus avancée et avec une propension plus élevée à donner des métastases. Outre sa fonction de réservoir d'énergie, l'adipocyte est une cellule endocrine active, capable de sécréter une grande variété de facteurs incluant, des chimiokines, des facteurs de croissance, des molécules pro-inflammatoires, qui peuvent réguler le comportement des cellules cancéreuses. Nous avons montré, que la co-culture en 2D, pendant 3 à 5 jours, de cellules tumorales avec des adipocytes, soit issus de la différenciation in vitro de la lignée murine 3T3-F442A, soit issus de la différenciation de précurseurs adipocytaires provenant de réductions mammaires, entrainait une augmentation des capacités invasives et migratoires des cellules tumorales, cet effet étant plus marqué pour des lignées faiblement invasives. Des expériences chez l'animal ont donné des résultats comparables. Les souris qui ont été injectées avec des 4T1 co-cultivées avec des adipocytes, présentent davantage de métastases pulmonaires que les souris qui ont été injectées avec des 4T1 non co-cultivées. Les adipocytes, quant à eux, lorsqu'ils sont co-cultivés avec les cellules tumorales, présentent un phénotype activé. .
The tumor progression was recently recognized as the product of a dynamic interaction between tumor cells and their microenvironment. Among the cells type which compose the microenvironment, adipocytes are the ones whose role was the least well characterized, in spite of the fact that adipocytes represent the main component of microenvironment in certain tumor models, as for example breast cancer, or the invasive prostate cancer. The role of fat cells in tumor progression has a great interest because it was demonstrated in epidemiological studies that the obesity is a factor of poor prognosis in numerous cancers. Indeed as shown the results of a vast study led by the Curie institute, patients affected by breast cancer, and who are obese, exhibit more aggressive tumors defined by a more advanced stage and/or lymph node involvment. Besides its function of energy storage, adipocyte is an endocrine cell, able to secrete a variety of molecules including, chemokines, growth factors, pro-inflammatory molecules, which can regulate the behavior of cancer cells. We have shown that the co-culture in 2D for 3 to 5 days, of tumoral cells with adipocytes (coming from in vitro differentiation of the murine cell line 3T3-F442A, or coming from the differentiation of precursors of mammary reductions), induce an increase of the invasive and migratory capacities of tumor cells, this effect being more marked for weakly invasive cell lines. Mice injected with 4T1 co-cultivated with adipocytes, exhibit more lung metastases than mice injected with 4T1 not co-cultivated. Adipocytes, in turn, when they are co-cultivated with the tumor cells, exhibit an activated phenotype. The secretion of pro-inflammatory markers as IL-6; IL-1 ß is increased, as well as an increase of metalloproteases as the MMP-11. IL-6, according to our results is involved in the modification of the phenotype of tumor cells, conferring them, an increase of the invasive capacities. Furthermore, these adipocytes acquire a fibroblastic phenotype that is characterized by a delipidation and a loss of markers of mature adipocytes, suggesting a reorientation of these cancer-associated adipocytes, which could contribute, by means of their secretions to the desmoplastic reaction observed in breast cancers. Furthermore, we also observed that free fatty acids released during the lipolysis of adipocytes, can be uptake and stored in lipid droplets by tumor cells. .

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Silva, Sandra Barbosa da. « Ciclagem da massa corporal em camundongos ». Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5953.

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Fundação Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro
A obesidade está associada com a inflamação crônica atribuída à liberação de citocinas e adipocinas, à homeostase desregulda da glicemia e à dislipidemia. Intervenções nutricionais são frequentemente acompanhadas por episódios repetidos de perda e recuperação do peso, fenômeno conhecido como efeito sanfona ou ciclagem da massa corporal. Foram avaliados os efeitos da ciclagem da massa corporal sobre os parâmetros: eficiência alimentar, massa corporal (MC), perfil lipídico, metabolismo de carboidratos, indíce de adiposidade corporal, marcadores inflamatórios, esteatose hepática e triglicerídeo (TG) hepático em camundongos C57BL/6 machos que ciclaram a massa corporal duas ou três vezes consecutivas pela alternância de dieta hiperlipídica (high-fat, HF) e dieta padrão (standard-chow,SC). Após cada ciclo de dieta HF, os animais ficavam cada vez mais pesados e, após cada ciclo de dieta SC, os animais perdiam cada vez menos peso. A ciclagem da massa corporal provocou flutuação nas reservas de gordura e nos lipídeos sanguíneos. O colesterol total dos animais, após mudança da dieta HF para dieta SC, apresentou redução dos seus valores, assim como os TG plasmáticos. No teste oral de tolerância à glicose, após o perído de ingestão da dieta HF, os animais apresentaram intolerância à glicose e, após a troca para dieta SC, os animais continuaram com intolerância à glicose. Em relação as adipocinas e citocinas, a leptina, resistina e o fator de necrose tumoral (TNF) alfa séricos aumentaram após o ciclo da dieta HF e diminuíram após a troca por dieta SC. Ao contrário, a adiponectina sérica diminuiu após dieta HF e aumentou após troca por dieta SC. A IL-6 aumentou após ingestão da dieta HF, porém após a troca para dieta SC, a IL-6 permaneceu elevada. Enquanto o MCP-1 não variou durante as trocas de dietas. A expressão da adiponectina no tecido adiposo diminuiu após a dieta HF e os valores permaneceram reduzidos mesmo após a troca para dieta SC. As expressões da leptina e IL-6 no tecido adiposo aumentaram após dieta HF e continuaram aumentados mesmo após a troca para dieta SC. Da mesma forma, a esteatose hepática e os TG hepáticos não reduziram após a mudança da dieta HF para dieta SC. Tanto a dieta HF, como a ciclagem da massa corporal são relevantes para o remodelamento do tecido adiposo e provoca repercussões nos lipídios séricos, na homeostase da glicose, na secreção de adipocinas e provoca acúmulo de gordura no fígado. A troca para dieta SC e redução da MC não são capazes de normalizar a secreção de adipocinas no tecido adiposo e nem das citocinas pró-inflamatórias que permaneceram aumentadas. A esteatose hepática e os TG hepáticos também não são recuperados com a troca para dieta SC e redução da massa corporal. Estes resultados indicam que a ciclagem da MC cria um ambiente inflamatório, que é agraado com adipocinas alteradas, intolerância à glicose e acúmulo de gordura no fígado
Obesity is associated with low-grade chronic inflammation attributed to release of cytokines and adipokines and to dysregulated glucose-insulin homeostasis and dyslipidemia. Nutritional interventions such as dieting are often accompanied by repeated bouts of weight loss and regain, a phenomenon known as weight cycling (WC). In this work we studied the effects of WC on the parameters: feed efficiency, body mass (BM), blood lipids, carbohydrate metabolism, adiposity, inflammatory markers, hepatic steatosis and hepatic triglyceride (TG) in C57BL/6 male mice that WC two or three consecutive times by alternation of a high-fat (HF) diet with standard chow (SC). The body mass (BM) grew up in each cycle of HF feeding, and decreased after each cycle of SC feeding. After three consecutive WC, less marked was the BM reduction during SC feeding, while more severe was the BM increase during HF feeding. After each cycle of the HF diet body mass grew up in each cycle of HF feeding, became increasingly heavier and after each cycle of SC feeding, the animals lost less weight. The WC mass caused fluctuations in fat reserves and blood lipids total cholesterol, after shift the HF diet by SC diet showed a reduction of their values and plasma TG. The oral glucose tolerance test after the regular intake of HF diet, the animals showed glucose intolerance and, after switching to SC diet, the animals continued with glucose intolerance. Regarding the adipokines and cytokines, leptin, resistin and tumor necrosis factor alpha (TNF) serum increased after the cycle of HF feeding and decreased after the switch to SC feeding. In contrast, serum adiponectin decreased after HF feeding and increased after dietary exchange for SC. The IL-6 increased after intake of HF diet, but after switching to SC feeding, which remained elevated, while the MCP-1 was not changed during the shift of diets. The expression of adiponectin in adipose tissue decreased after the HF feeding and the values remained low even after switching to diet SC. The expression of leptin, IL-6 in the adipose tissue increased after HF feeding and remained elevated after the change to SC diet. Similarly, hepatic steatosis, and hepatic TG not reduced after the change to the diet HF diet SC. The results of the present study showed that both the HF diet and WC are relevant to BM evolution and fat pad remodeling in mice, with repercussion in blood lipids, homeostasis of glucose-insulin, adipokine levels and causes fat accumulation in the liver. The simple reduction of the BM during a WC is not able to recover the high levels of adipokines in the adipose tissue and serum as well as the pro-inflammatory cytokines. Hepatic steatosis and hepatic TG are not recovered with the change to SC feeding and body mass reduction. These findings indicate that the WC creates an inflammatory environment; with altered adipokines in association with WC which potentially aggravates the chronic inflammation attributed to dysregulated production and release of adipokines in mice

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Oliveira, Liliane Soares Corrêa de. « Dieta rica em sacarose : perfil inflamatório e danos hepáticos em camundongos ». Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6922.

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Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro
Ainda não está bem definido na literatura se uma dieta rica em sacarose, mesmo sendo isoenergética, provoca danos à saúde. Camundongos C57BL/6 foram alimentados com uma dieta controle (10% da energia proveniente de gordura, 8% da energia proveniente da sacarose - SC), uma dieta rica em sacarose (10% de energia proveniente da gordura, 32% da energia proveniente da sacarose - HSu), uma dieta hiperlipídica (42% da energia proveniente de gordura, 8% da energia proveniente da sacarose - HF) ou uma dieta combinada HF/HSu (42% da energia proveniente de gordura, 32% da energia proveniente da sacarose), durante oito semanas. Apesar da massa corporal e do índice de adiposidade não terem sofrido alteração, o grupo HSu apresentou hipertrofia dos adipócitos, o que também foi observado nos grupos HF e HF/HSu. Os grupos HF, HSu e HF/HSu foram intolerantes à glicose e apresentaram níveis séricos de insulina elevados. Os níveis séricos de leptina, resistina e proteína quimiotática de monócitos-1 (MCP-1) aumentaram, enquanto adiponectina sérica reduziu nos grupos HF, HSu e HF/HSu. No tecido adiposo, os animais HF, HSu e HF/HSu apresentaram maiores níveis de expressão protéica de leptina e níveis mais baixos de expressão protéica de adiponectina, em comparação ao grupo SC. Colesterol hepático foi maior nos grupos HF e HF/HSu, enquanto TG hepático foi maior nos grupos HSu e HF/HSu. Os animais dos grupos HF, HSu e HF/HSu apresentaram esteatose hepática, aumento da expressão protéica hepática de elemento regulador de esterol ligante da proteína 1 (SREBP-1c) e diminuição da expressão protéica do receptor ativador de proliferação peroxissomal alfa (PPAR-α). Em conclusão, a dieta rica em sacarose não provoca obesidade nos animais, mas provoca alterações nos adipócitos (hipertrofia), intolerância à glicose, hiperinsulinemia, hiperlipidemia, esteatose hepática e aumento de citocinas inflamatórias. Os efeitos prejudiciais da dieta rica em sacarose, mesmo quando a sacarose substitui isocaloricamente o amido na alimentação, pode ter consequências para a saúde.
It is still unclear if an isoenergetic, sucrose-rich diet leads to health conse-quences. Mice were fed a control diet (10% energy from fat, 8% energy from sucrose - SC), a high-sucrose diet (10% energy from fat, 32% energy from sucrose - HSu), a high-fat diet (42% energy from fat, 8% energy from sucrose - HF) or a HF/HSu diet (42% energy from fat, 32% energy from sucrose) for eight weeks. Despite the un-changed body mass and adiposity indices, HSu presented adipocyte hypertrophy, which was also observed in the HF and HF/HSu. The HF, HSu and HF/HSu were glucose intolerant and had elevated serum insulin levels. The levels of leptin, resistin and Monocyte Chemotactic Protein-1 (MCP-1) increased, while the serum adiponectin decreased in the HF, HSu and HF/HSu. In the adipose tissue, the HF, HSu and HF/HSu showed higher levels of leptin protein expression and lower levels of adiponectin protein expression in comparison with the SC. Hepatic cholesterol was higher in the HF and HF/HSu, while hepatic TG was higher in the HSu and HF/HSu. Liver steatosis was higher, sterol regulatory element-binding protein-1c (SREBP-1c) hepatic expression was increased, and peroxisome proliferator-activated receptor-alpha (PPAR-α) hepatic protein expression was decreased in the HF, HSu and HF/HSu in comparison with the SC. In conclusion, a sucrose-rich diet does not lead to a state of obesity but has the potential to cause changes in the adipocytes (hypertrophy) as well as glucose intolerance, hyperinsulinemia, hyperlipidemia, hepatic steatosis, and increases in the number of inflammatory cytokines. The deleterious effects of a sucrose-rich diet in an animal model, even when the sucrose replaces starch isocalorically in the feed, can have far-reaching consequences for health.

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Persdotter, Hedlund Gabriella. « Protein and mRNA Studies of Rat FA1/Pref-1/dlk ». Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7773.

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Κωστόπουλος, Χρήστος. « Μελέτη της έκφρασης λιποκινών και των υποδοχέων τους σε περιαγγειακό λιπώδη ιστό ανθρώπου και συσχέτιση με την αθηροσκλήρωση ». Thesis, 2014. http://hdl.handle.net/10889/8535.

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Ο λιπώδης ιστός θεωρείται πλέον ενδοκρινές όργανο που παράγει πληθώρα βιολογικά δραστικών πεπτιδίων, που καλούνται λιποκίνες. Ανάλογα με την ανατομική τους εντόπιση, οι διαφορετικές αποθήκες λίπους έχουν και διαφορετική ικανότητα παραγωγής λιποκινών και επίδρασης σε φυσιολογικές λειτουργίες. Οι λιποκίνες που παράγονται από τον περιαγγειακό λιπώδη ιστό εμπλέκονται στην παθογένεια αγγειακών νόσων, συμπεριλαμβανόμενης της αθηροσκλήρωσης. Είναι γνωστό πως η αντιπονεκτίνη ασκεί αντιαθηρογόνες δράσεις, ενώ ο ρόλος της Τ-καντχερίνης ως υποδοχέα της αντιπονεκτίνης δεν έχει πλήρως διαλευκανθεί. Το απελινεργικό σύστημα, αποτελούμενο από την απελίνη και τον υποδοχέα της APJ, αποτελεί μεσολαβητή ποικίλων καρδιαγγειακών λειτουργιών και ενδέχεται να συμμετέχει και στην αθηροσκληρωτική διαδικασία. Η χεμερίνη είναι λιποκίνη με γνωστό ρόλο στην ανοσία, στη λειτουργία του λιπώδους ιστού και στο μεταβολισμό, δρώντας κυρίως μέσω του υποδοχέα της CMKLR1. Μελετήσαμε την πρωτεϊνική έκφραση της αντιπονεκτίνης και της Τ-καντχερίνης, της απελίνης και του APJ, της χεμερίνης και του CMKLR1 σε ανθρώπινες αορτές, στεφανιαίες αρτηρίες και στον αντίστοιχο περιαγγειακό λιπώδη ιστό και συσχετίσαμε την έκφρασή τους με την παρουσία αθηροσκλήρωσης και με κλινικές παραμέτρους. Εφαρμόστηκε ανοσοϊστοχημική χρώση για την αντιπονεκτίνη, την Τ-καντχερίνη, την απελίνη, τον APJ, τη χεμερίνη και τον CMKLR1 σε δείγματα ανθρώπινων αορτών και στεφανιαίων αρτηριών, περιλαμβανόμενου και του περιαγγειακού λίπους. Οι αορτικές και στεφανιαίες αθηρωματικές βλάβες αξιολογήθηκαν με βάση την κατάταξη του AHA. Ανοσοϊστοχημική χρώση, ποικίλης έντασης, για την αντιπονεκτίνη ανιχνεύθηκε μόνο στα λιποκύτταρα, ενώ η Τ-καντχερίνη εντοπίστηκε στα αγγειακά λεία μυικά κύτταρα (ΑΛΜΚ) και στα ενδοθηλιακά κύτταρα. Ανοσοϊστοχημική χρώση για την απελίνη ανιχνεύθηκε σε λιποκύτταρα, ΑΛΜΚ, ενδοθηλιακά κύτταρα και μακροφάγα-αφρώδη κύτταρα των αθηρωματικών βλαβών, ενώ ο APJ εντοπίστηκε στα ΑΛΜΚ και στο ενδοθήλιο των αγγείων. Ανοσοθετικότητα για τη χεμερίνη παρατηρήθηκε και στις δύο αποθήκες λίπους ,στα ΑΛΜΚ και σε αφρώδη κύτταρα των αθηρωματικών βλαβών. Ο CMKLR1 εκφράστηκε σε ΑΛΜΚ και σε αφρώδη κύτταρα αορτών και στεφανιαίων αγγείων με αθηρωματικές βλάβες. Η έκφραση αντιπονεκτίνης στον περιαγγειακό λιπώδη ιστό και η έκφραση Τ-καντχερίνης στα ΑΛΜΚ συσχετίστηκαν αρνητικά με την αθηροσκλήρωση και στις δύο εντοπίσεις, όπως και η έκφραση απελίνης στα ΑΛΜΚ. Η έκφραση χεμερίνης στις περιαγγειακές αποθήκες λίπους και στα αφρώδη κύτταρα συσχετίστηκε στατιστικά σημαντικά με τη βαρύτητα της αθηροσκλήρωσης και στις δύο εντοπίσεις. Πολλές ακόμα – ειδικές για την εντόπιση – συσχετίσεις παρατηρήθηκαν. Τα αποτελέσματά μας υποδεικνύουν πιθανό ρόλο της Τ-καντχερίνης ως μεσολαβητή των αντιαθηρογόνων δράσεων της αντιπονεκτίνης, ενώ υποστηρίζουν το ενδεχόμενο αντιαθηρογόνο προφίλ της απελίνης και του υποδοχέα της APJ στις ανθρώπινες αρτηρίες. Ενισχύουν, ακόμα, τον υποτιθέμενο ρόλο της χεμερίνης στην εξέλιξη των αθηρωματικών βλαβών, πιθανότατα δρώντας μέσω του CMKLR1 υποδοχέα της. Περαιτέρω έρευνα είναι αναγκαία για να αποσαφηνιστεί ο ρόλος της τοπικά παραγόμενης αντιπονεκτίνης, απελίνης και χεμερίνης και της σηματοδότησης μέσω των αντίστοιχων υποδοχέων τους – T-cadherin, APJ και CMKLR1 – στην παθογένεια της αθηροσκλήρωσης στον άνθρωπο.
Adipose tissue is considered an endocrine organ, producing numerous bioactive peptides, called adipokines. Depending on their anatomical location, different fat depots have a different capacity to produce adipokines and influence physiological functions. Adipokines produced by periadventitial fat have been implicated in the pathogenesis of vascular disease, including atherosclerosis. Adiponectin has established anti-atherogenic actions, while the role of T-cadherin as an adiponectin receptor is not fully elucidated. The apelinergic system, consisting of apelin and its APJ receptor, is a mediator of various cardiovascular functions and may also be involved in the atherosclerotic process. Chemerin is an adipokine with an established role in immunity, adipose tissue function and metabolism, acting, mainly through its CMKLR1 receptor. We investigated the protein expression of adiponectin and T-cadherin, apelin and APJ, chemerin and CMKLR1 in human aortas, coronary vessels and the respective periadventitial adipose tissue and correlated their expression with the presence of atherosclerosis and clinical parameters. Immunohistochemistry for adiponectin, T-cadherin, apelin, APJ, chemerin and CMKLR1 was performed on human aortic and coronary artery samples including the periadventitial adipose tissue. Aortic and coronary atherosclerotic lesions were assessed using the AHA classification. Adiponectin immunostaining, of varied intensity, was detected only in adipocytes, while T-cadherin was localized to vascular smooth muscle cells (VSMCs) and endothelial cells. Apelin immunostaining was detected in adipocytes, VSMCs, endothelial cells and foam cells in atherosclerotic lesions, while APJ was found in VSMCs and endothelia. Chemerin immunopositivity was noticed in both periadventitial fat depots, in VSMCs and foam cells in atherosclerotic lesions. CMKLR1 was expressed in VSMCs and foam cells in aortic and coronary vessels with atherosclerotic lesions. Periadventitial adiponectin and VSMC T-cadherin expression were negatively correlated with atherosclerosis in both sites, as was VSMC apelin expression. Chemerin expression in periadventitial fat depots and foam cells was statistically significantly correlated with the severity of atherosclerosis in both locations. Several other – depot specific – associations were observed. Our results suggest a possible role for T-cadherin as a mediator of anti-atherogenic adiponectin actions, while they support the putative anti-atherogenic profile for apelin and its APJ receptor in human arteries. They also lend some support to a presumable role of chemerin in the progression of atherosclerotic lesions, possibly acting through its CMKLR1 receptor. Further research is necessary to elucidate the role of locally produced adiponectin, apelin and chemerin and signaling through their respective receptors – T-cadherin, APJ and CMKLR1 – in the pathogenesis of human atherosclerosis.

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Payne, Gregory Allen. « Contribution of Perivascular Adipose Tissue to Coronary Vascular Dysfunction ». Thesis, 2011. http://hdl.handle.net/1805/2490.

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Indiana University-Purdue University Indianapolis (IUPUI)
The epidemic of obesity and associated cardiovascular complications continues to grow at an alarming rate. Currently, obesity is thought to initiate a state of chronic inflammation, which if unresolved potentially causes cardiovascular dysfunction and disease. Although poorly understood, release of inflammatory mediators and other cytokines from adipose tissue (adipocytokines) has been proposed to be the molecular link between obesity and coronary artery disease. Furthermore, the anatomic location of adipose has been increasingly recognized as a potential contributor to vascular disease. Importantly, the development of coronary atherosclerosis, a key component of heart disease, is typically found in segments of coronary arteries surrounded by perivascular adipose tissue. Accordingly, the goal of this project was to determine how perivascular adipose tissue affects coronary artery function and elucidate the critical mechanisms involved. Initial studies assessing arterial function were conducted with and without perivascular adipose tissue. Preliminary results demonstrated that factors released by perivascular adipose tissue effectively impaired coronary endothelial function both in vitro and in vivo. This observation was determined to be caused by direct inhibition of nitric oxide synthase (NOS), a critical enzyme for the production nitric oxide. Attenuation of endothelium-dependent vasodilation was independent of changes in superoxide production, smooth muscle response, or peroxide-mediated vasodilation. Additional studies revealed that perivascular adipose-induced impairment of NOS was due to increased inhibitory regulation by the β isoform of protein kinase C (PKC-β). Specifically, perivascular adipose-derived factors caused site specific phosphorylation of nitric oxide synthase at Thr-495. Additional experiments investigated how perivascular adipose-derived factors contributed to coronary artery disease in an animal model of obesity. Results from these studies indicated that perivascular adipose-derived leptin markedly exacerbated underlying endothelial dysfunction, and significantly contributed to coronary endothelial dysfunction through a PKC-β dependent mechanism. Findings from this project confirm epicardial perivascular adipose tissue as a local source of harmful adipocytokines. In addition, perivascular adipose-derived leptin was demonstrated to be a critical mediator of coronary vascular dysfunction in obesity. Together, the results strongly suggest that perivascular adipose tissue is a key contributor to coronary artery disease in obesity.

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Eschholz, Norman. « Untersuchung der systemischen und parakrinen Wirkungen von Leptin auf die Neointimabildung nach experimenteller Gefäßverletzung im Mausmodell ». Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-0028-871E-3.

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Zieger, Konstanze, Juliane Weiner, Kerstin Krause, Maximilian Schwarz, Martin Kohn, Michael Stumvoll, Matthias Blüher et John T. Heiker. « Vaspin suppresses cytokine-induced inflammation in 3T3-L1 adipocytes via inhibition of NFκB pathway ». 2018. https://ul.qucosa.de/id/qucosa%3A33206.

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Vaspin expression is increased in white adipose tissue (WAT) of diet-induced obese mice and rats and is supposed to compensate HFD-induced inflammatory processes and insulin resistance in adipose tissue by counteracting pro-inflammatory gene expression in obesity. Multiple studies have also demonstrated strong anti-inflammatory effects in vascular and skin cells. Here, we used vaspin treated 3T3-L1 murine adipocytes as well as 3T3-L1 cells with stable vaspin expression to investigate the effect of exogenous and endogenous vaspin on inflammatory processes and insulin signaling in adipocytes. Our stably transfected cells secreted significant amounts of vaspin which was in the physiological range of ∼0.5 ng/ml in cell supernatants. Adipocyte differentiation was not affected by vaspin as expression of adipogenic marker genes as well as lipid accumulation after full differentiation was similar to control cells. We found that IL-1β induced expression and secretion of pro-inflammatory cytokines, such as IL-6, MCP1 and TNFα was significantly blunted in vaspin expressing 3T3-L1 cells. Treatment of 3T3-L1 cells with exogenous vaspin resulted in reduced cytokine-induced activation of the intracellular and pro-inflammatory NFκB signaling cascades (IKKα/β, IκB and NFκB). Moreover, endogenous vaspin positively affected insulin signaling by increasing insulin-stimulated phosphorylation of the key mediator protein kinase B (AKT). Together, we demonstrate anti-inflammatory effects of vaspin in 3T3-L1 adipocytes as well as increased insulin signaling by endogenous expression or exogenous treatment. The results provide evidence for potent anti-inflammatory action of vaspin not only in vascular cells but also in adipose tissue.

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Teng, I.-Hsuan, et 滕旖萱. « Adipokine expression profiles of adipose tissues in dogs ». Thesis, 2019. http://ndltd.ncl.edu.tw/cgi-bin/gs32/gsweb.cgi/login?o=dnclcdr&s=id=%22107NCHU5541017%22.&searchmode=basic.

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碩士
國立中興大學
獸醫學系暨研究所
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White adipose tissues (WATs) produce a variety of bioactive peptides, collectively termed adipokines. Some adipokines have been known to regulate insulin sensitivity, such as adiponectin, interleukin-6 (IL-6), resistin and leptin. In human, studies have confirmed that obesity is accompanied by original adipocytes enlargement, which results in dysregulated adipokine levels and predisposes to the development of type 2 diabetes mellitus (T2DM). Unlike human, T2DM is a rare metabolic disease in dogs. Most clinically recognized form of DM in dogs resembles T1DM in human. However, the underlying mechanisms of low prevalence of T2DM in dogs remain rarely discussed. Since adipokine expression profiles between lean and obese WATs are crucial to the development of T2DM in human, analyses and comparison of adipokine expression between lean and obese dogs might provide some clues to better understand this clinical presentation. Previous study indicated that lipoma seems to have the similar feature of adipokine secretion as normal WATs. Therefore, the purpose of this study was to assay and compare the expression of adipokines in lean and obese dogs with WATs and lipomas. This study included 24 dogs undergoing lipoma resection in Veterinary Medical Teaching Hospital of National Chung Hsing University during 2016 to March 2019, and the lipoma specimens together with peritumoral WATs and preoperative fasting blood samples are all collected for analysis. Investigated the mRNA expression of adipokines in adipose tissue using reverse transcription-polymerase chain reaction (RT-PCR). In additional, fasting glucose, insulin, and adiponectin concentrations in plasma were also be detected. The results showed that the levels of expression of adiponectin, leptin, and IL-6 in lipomas and normal WATs as well as fasting glucose levels (p = 0.839) and plasma adiponectin (p = 0.106) were not reaching statistically significant differences between lean and obese dogs. However, fasting insulin (p = 0.034) and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) calculated values (p = 0.031) were reaching statistically significant difference between two groups, it showed that there was significant higher insulin levels and insulin resistance (IR) in obese dogs. There was no obvious variations in adipocytes size between the lean and obese groups comparison of within normal WATs (p = 0.992) or lipomas (p = 0.067). However, the size of adipocytes in lipomas in the obese group was significantly larger than the adipocytes in the lean group (p = 0.002) and obese group (p = 0.007) in normal WATs. Because of the critical roles of obesity-induced IR and dysregulated adipokines in the development of T2DM in humans, our findings suggest that the dysregulation of adipokines was not observed in obese dogs. Although IR were presented in obese state, the hyperinsulinemia was still effective compensation response to maintain glucose homeostasis. Thus, the inert adipokine dynamics may be the putative mechanism to the low prevalence of T2DM in the obese dogs.

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Courtois-Allard, Myriam. « L'effet du bagage génétique des souris C57BL/6 et SJL sur les niveaux d'adipokines par les différents dépôts du tissu adipeux ». Mémoire, 2010. http://www.archipel.uqam.ca/2824/1/M11312.pdf.

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L'obésité est une maladie multifactorielle dont la génétique semble être un acteur prédominant dans le développement de cette maladie. Malgré de nombreuses études qui sont à la recherche des polymorphismes responsables de cette maladie, très peu d'études ont vérifié si les profils d'adipokines des différents dépôts adipeux étaient affectés par le bagage génétique. Cette étude a émis comme hypothèse que le bagage génétique était un acteur important dans le processus d'inflammation causé par l'obésité. Deux souches de souris femelles ont été étudiées soient la C57BL/6 et la SJL. La souris SJL est une souris résistante à la nourriture riche en lipides i.e. qu'elle ne développe pas de surpoids relié à sa consommation contrairement à la C57BL/6. Conséquemment, le profil d'adipokines de la souris SJL ne devrait pas être affecté par ce régime. Les souris C57BL/6 et SJL ont été nourries pendant 12 semaines avec un régime riche en lipides. Les marqueurs d'inflammation suivant: le TNF-α, l'IL-6, la leptine, l'adiponectine, l'IL-10 et le TGF-β1 ont été dosés par ELISA. La nourriture HTL n'a pas entraîné de surpoids chez aucune des deux souches. Cependant, le profil d'adipokines de la souris C57BL/6 est affecté par la nourriture riche en lipides. Dans le tissu MES, la quantité de TNF-α, IL-6, leptine, adiponectine et IL-10 est significativement plus élevée comparativement aux quantités retrouvées chez les souris témoins. Cette donnée suggère qu'une nourriture riche en lipides est capable d'induire des changements dans le métabolisme du tissu adipeux. Bref, le métabolisme du tissu adipeux serait régulé par d'autres facteurs que l'obésité. Chez SJL, les niveaux d'adipokines ne sont pas affectés par la nourriture riche en lipides comparativement aux souris témoin excepté pour l'adiponectine. Il ya une diminution de l'adiponectine dans le tissu ING et MES. Les réponses différentes à une nourriture riche en lipides pourraient s'expliquer par les niveaux d'adiponectine. L'adiponectine est une hormone anti-inflammatoire et sa quantité est 100X plus élevée chez la souris SJL que chez C57BL/6. Chez la souris SJL, la quantité élevée d'adiponectine pourrait jouer un rôle protecteur contre l'inflammation. En conclusion, cette étude suggère que le bagage génétique a une influence sur le profil d'adipokine. ______________________________________________________________________________ MOTS-CLÉS DE L’AUTEUR : Adipokine, Pro-inflammatoire, Anti-inflammatoire, Tissu adipeux, Inguinal, Mésentérique, Paramétrial, TNF-α, IL-6, Leptine, IL-10, Adiponectine, TGF-β, C57BL-6 et SJL.

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Tan, Paul. « Mécanismes impliqués dans les effets du récepteur à la (pro)rénine sur le développement de l'obésité et de ses complications cardiométaboliques associées ». Thèse, 2015. http://hdl.handle.net/1866/13532.

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L'obésité est une maladie associée à de nombreuses complications comme le diabète de type 2, l'hypertension et le cancer. De nos jours, les modifications au mode de vie, tels l’alimentation et le niveau d’activité physique, ne sont pas suffisants pour combattre les effets délétères de l'obésité. La pharmacothérapie est un traitement alternatif bien que les effets bénéfiques soient temporaires et ne peuvent être maintenus à long terme. Le besoin pour un traitement bénéfique à long terme sans effet secondaire n'est pas comblé. Mieux connu pour son rôle dans la régulation de la pression artérielle, le système rénine-angiotensine favorise l'entreposage du gras. Le récepteur à la prorénine et à la rénine est une composante du système rénine-angiotensine. Ainsi, le récepteur qui amplifie l'activation de celui-ci pourrait avoir un rôle clé dans le gain de masse grasse. Le but de ce projet de thèse est d'évaluer le rôle du récepteur à la prorénine et à la rénine dans le développement de l'obésité et de ses complications chez la souris et ce, en utilisant une combinaison de diète riche en gras et en hydrates de carbone et du handle region peptide, un bloqueur du récepteur à la prorénine à la rénine. Après une période de 10 semaines, nous avons constaté que l'expression et la protéine du récepteur à la prorénine et à la rénine augmentent spécifiquement dans le tissu adipeux sous-cutané et viscéral des souris obèses. Lorsqu'administré en concomitance avec une diète riche en gras et en hydrates de carbone, le handle region peptide favorise chez la souris des diminutions des gains des masses corporelles et adipeuses viscérales. Une diminution de l'expression de l'enzyme catalysant la dernière étape de la lipogenèse pourrait être responsable de la réduction de gras viscéral. Chez les mêmes animaux, l'expression de plusieurs adipokines est également diminuée dans le tissu adipeux suggérant une réduction de la résistance à l'insuline, de l'inflammation et de l'infiltration des macrophages localement dans le gras sous-cutané et viscéral. L'augmentation de l'expression d’un marqueur de l'adipogenèse dans le tissu adipeux sous-cutané pourrait suggérer un plus grand nombre d'adipocytes. Cela pourrait tamponner l'excès d'acides gras libres circulants puisque nous avons constaté une diminution de ce paramètre chez les souris ayant une diète riche en gras et en hydrates de carbone et traitées avec le peptide. Nous avons émis l'hypothèse qu'un cycle futile pourrait être activé dans le gras sous-cutané car nous avons observé une augmentation de l'expression de plusieurs enzymes impliquées dans la lipogenèse et dans la lipolyse. Le ''brunissement'' du tissu adipeux est la présence de cellules similaires aux adipocytes bruns dans le tissu adipeux qui sont caractérisés par une grande densité mitochondriale et la thermogenèse. L'augmentation de l'expression des marqueurs de ''brunissement'' et de biogenèse de mitochondrie dans le gras sous-cutané suggère que le ''brunissement'' pourrait également être activé dans ce dépôt de gras. La sensibilité à l'insuline chez ces animaux pourrait être améliorée telle que suggérée en circulation par la diminution de l'insuline, par le glucose qui change peu, par l'augmentation du ratio glucose sur insuline ainsi que par un changement potentiel dans la corrélation entre le poids corporel de la souris et les niveaux d’adiponectine circulante. Nos travaux suggèrent que le handle region peptide pourrait augmenter la capacité du tissu adipeux sous-cutané à métaboliser les lipides circulants avec l'activation potentielle d'un cycle futile et le ''brunissement''. Cela préviendrait le dépôt ectopique de lipides vers les compartiments viscéraux comme le suggère la réduction de masse adipeuse viscérale chez les souris ayant une diète riche en gras et en hydrates de carbone et traitées avec le peptide. Utilisant un modèle de souris, cette étude démontre le potentiel pharmacologique du handle region peptide comme un nouveau traitement pour prévenir l'obésité.
Obesity is a disease associated with multiple complications such as type 2 diabetes, hypertension and cancer. Nowadays, lifestyle modifications, such as eating habits and physical activity, are simply not enough to counter the deleterious effects of obesity. Pharmacotherapy is used as an alternative treatment although beneficial effects are temporary and cannot be maintained in the long run. The current medical need for a treatment with long term beneficial outcomes devoid of side effects is unmet. Best known for its role in blood pressure regulation, the renin-angiotensin system has recently been attributed a role in favouring fat storage. The prorenin and renin receptor is a component of renin-angiotensin system that amplifies its activation. Thus, the prorenin and renin receptor might play a key role in gaining fat mass. The aim of this thesis is to investigate the role of the prorenin and renin receptor in the development of obesity and its complications in mice using a combination of high-fat and high carbohydrate diet and the handle region peptide, a blocker of the prorenin and renin receptor. After a period of 10 weeks, we have found that the prorenin and renin receptor is increased specifically in subcutaneous and visceral adipose tissue of obese mice. When administered simultaneously with a high-fat and high-carbohydrate diet, the handle region peptide reduced body weight gain in mice with similar decrease in visceral fat mass. Decreased expression of the enzyme catalyzing the last step of lipogenesis could be responsible for the reduction in visceral fat mass. In the same animals, the expressions of several adipokines were also decreased in adipose tissue suggesting reduced insulin resistance, inflammation and macrophage infiltration locally in subcutaneous and visceral fat. Increased expression of a marker of adipogenesis in subcutaneous adipose tissue could suggest higher adipocyte number. This would buffer excess circulating free fatty acid since we have noticed a reduction in the latter in mice on a high-fat and high-carbohydrate diet and treated with the peptide. We hypothesized that a futile cycle could be activated in subcutaneous fat because we have observed increased expression of several enzymes implicated in lipogenesis and lipolysis. « Beiging » is defined as the presence of brown-like adipocytes in adipose tissue which is characterized by high mitochondrial density and thermogenesis. Increased expression of markers for « beiging » and mitochondrial biogenesis in subcutaneous fat suggests that « beiging » could also be activated in this fat pad. Insulin sensitivity in these animals could be improved as suggested in the circulation by decreased insulin, similar glucose, increased glucose on insulin ratio as well as a possible change in the correlation between mouse body weight and circulating adiponectin levels. Our work suggests that the handle region peptide could increase the capacity of subcutaneous adipose tissue to metabolize circulating lipids with a potential activation of a futile cycle and « beiging ». This would prevent ectopic deposition of fat in visceral compartments as suggested by the reduction in visceral fat mass in mice on high-fat and high-carbohydrate diet and treated with the peptide. Using a mice model, this study demonstrates the pharmacological potential of the handle region peptide as a novel treatment to prevent obesity.

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Knebusch, Toriello Stefanie. « Depot differences in adipokine secretion from human omental and abdominal subcutaneous adipose tissues : potential role of adiporedoxin ». Thesis, 2015. https://hdl.handle.net/2144/13961.

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Adiporedoxin (Adrx) is an adipose tissue specific protein discovered by the Pilch lab. It is a member of the peroxiredoxin family localized in the endoplasmic reticulum (ER). Previous studies showed that Adrx is involved in ER redox regulation and disulfide bond formation and secretion of adipokines. Further, Adrx mRNA expression and protein levels in human abdominal adipose tissue of young, healthy subjects, ranging in levels of obesity, correlated positively with adiponectin mRNA and protein, and negatively with adipose tissue inflammation (as indicated by phospho-Jun kinase). Since previous studies have shown depot differences in adipokine release, we wanted to determine the differences on adipose tissues depot in Adrx expression. However, there are no data on depot differences in Adrx expression and its association with changes in adipokine release in human adipose tissue. It is well known that omental adipose tissue is more inflamed, and reports on depot differences in adipokine release, especially adiponectin are inconsistent however leptin and IL-6 have being consistent. Adipokine release measured from adipose tissues reflects a more physiologic state and the characteristics of the subjects compared to cultured cells. Adiponectin is an insulin sensitizing protein, exclusively produced by mature adipocytes and highly secreted by adipose tissue. The native adiponectin exists as low molecular weight, middle-molecular weight and high molecular weight (HMW).The potency of adiponectin is linked to the HMW isoform. There are no previous reports on secretion of HMW adiponectin from human omental (Om) and abdominal subcutaneous (Abdsc) adipose tissues. In this study the goal is to determine the depot differences in Adrx expression and adipokine release in human Abdsc and Om adipose tissue in obese and morbidly obese subjects, mostly females and to determine the relationship between Adrx protein expression and adipokine release in Abdsc versus Om and circulating levels of adipokines, primarily total and HMW adiponectin. To clarify whether Adrx expression is implicated in the release and secretion of circulating adipokines. Adrx protein levels (assessed by Western blot) were ~1.4 fold higher in Abdsc than Om (p<0.05; paired t-test values). As expected, secretion per gram of tissue in 3hr incubation of total adiponectin (~ 25%) and leptin (~50%) was higher, and IL-6 secretion was lower (~30%) in Abdsc compared to Om. In western blot, total adiponectin is higher in Abdsc compared to Om. However, HMW adiponectin and % HMW are higher in Om. Adrx protein levels were positively correlated with total adiponectin and HMW release in Abdsc and only with HMW in Om. Adrx levels were negatively correlated with % HMW in Abdsc but not in Om. Adrx protein levels in Abdsc showed a negative trend with total adiponectin circulating levels (ng/ml measured by ELISA) and a positive trend in Om. However, total adiponectin by Western Blot showed a positive trend with Adrx levels in both Abdsc and Om. HMW adiponectin levels tended to be slightly positive with Adrx levels in Abdsc and Om. However, the percent of HMW adiponectin levels are not correlated with Adrx levels in either tissues. Since in Adrx KO mice found that presented lower total adiponectin in circulation, it was hypothesized that Adrx were positively correlated with circulating adiponectin, and wanted to study the correlation with serum adipokines. However, none of the correlations with Adrx and adipokines in serum were statistically significant. These data suggest that depot differences in Adrx expression may influence depot differences in adipokine secretion. The mechanism of higher HMW adiponectin secretion in Om with low Adrx levels needs further study.

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Tishinsky, Justine. « Modulation of Adipokines by n-3 Polyunsaturated Fatty Acids and Ensuing Changes in Skeletal Muscle Metabolic Response and Inflammation ». Thesis, 2012. http://hdl.handle.net/10214/3778.

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Adipose tissue represents an important endocrine organ that secretes a multitude of adipokines known to mediate inflammation, lipid metabolism, and insulin sensitivity in peripheral tissues such as skeletal muscle. Specifically, adiponectin stimulates skeletal muscle fatty acid oxidation and is associated with improvements in insulin response. Long-chain n-3 polyunsaturated fatty acids (PUFA) are well known for their anti-inflammatory and insulin-sensitizing properties, and their dietary consumption is associated with a more favourable circulating adipokine profile, including increased adiponectin. However, whether n-3 PUFA can directly stimulate adiponectin secretion from human adipocytes, as well as the underlying mechanisms involved, is unknown. In contrast to n-3 PUFA, diets high in saturated fatty acids (SFA) are thought to decrease adiponectin and increase pro-inflammatory adipokines, as well as blunt skeletal muscle response to both adiponectin and insulin, possibly via activation of inflammatory pathways. The role of n-3 PUFA in mediating the communication between adipose tissue and skeletal muscle, as well as preventing SFA-induced impairments in skeletal muscle function, has yet to be examined. In this thesis, it was found that long-chain n-3 PUFA increase adiponectin secretion from human adipocytes via a peroxisome proliferator-activated receptor gamma-dependent mechanism. The effects of n-3 PUFA on adiponectin secretion were additive when combined with the thiazolidinedione, rosiglitazone. Secondly, incorporation of n-3 PUFA into a high SFA diet prevented impairments in adiponectin response and both prevented and restored impairments in insulin response in rodent skeletal muscle. Interestingly, these findings were paralleled by prevention of SFA-induced increases in toll-like receptor 4 expression by n-3 PUFA, suggesting inflammatory changes may be involved. Finally, dietary n-3 PUFA and SFA modulated the secretion of adipose tissue-derived factors from visceral rodent adipose tissue and subsequent exposure of isolated skeletal muscle to such factors induced acute changes in inflammatory gene expression without affecting insulin sensitivity. Together, the findings in this thesis suggest that n-3 PUFA modulate adipokine secretion from adipose tissue and that adipose-derived factors mediate skeletal muscle inflammation and response to adiponectin and insulin. Ultimately, this work highlights the importance of considering n-3 PUFA as a therapeutic strategy in the prevention and treatment of obesity and related pathologies.

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Klímová, Judita. « Úloha tukové tkáně v rozvoji inzulinorezistence a dalších metabolických změn u nemocných s feochromocytomem ». Doctoral thesis, 2021. http://www.nusl.cz/ntk/nusl-448045.

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Pheochromocytoma and functional paraganglioma (PPGL) are rare neuroendocrine tumors characterized by catecholamines overproduction, which give a rise to disorders of glucose, lipid, and energy metabolism. The role of adipose tissue in these processes remains unclear. Our aim was to determine the gene expression profile in subcutaneous and visceral adipose tissue of patients with PPGL focusing on endocrine functions of adipose tissue, occurrence of brown (BAT) and beige adipose tissue (BeAT), all in connection with other measured metabolic and energy parameters and levels of circulating adipokines. We demonstrate signs of UCP1-dependent norepinephrine induced thermogenesis connected with overexpression of DIO2 in retroperitoneal VAT of PPGL and higher expression of key transcriptional factors of brown/beige adipogenesis, namely PPARGC1α, CEBPB and PRDM16. However, classic murine BAT or BeAT gene signature in VAT of PPGL was not detected. In subcutaneous adipose tissue (SAT) of PPGL we found signs of possible BeAT transformation, however without simultaneously undergoing UCP1-dependent thermogenesis. We also demonstrate that patients with PPGL have higher serum levels of FGF21 compared to healthy controls and these levels do not differ from obese patients. Furthermore, successful tumor removal...

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Cheng, Kai-Hung, et 鄭凱鴻. « Inflammatory markers and adipokines of abdominal, pericardial and peripheral fat tissues in patients with coronary artery disease ». Thesis, 2006. http://ndltd.ncl.edu.tw/handle/84818696532648546404.

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碩士
高雄醫學大學
醫學研究所碩士班
94
Background—It has been shown that inflammatory mediators in epicardial fat is higher than subcutaneous adipose stores in patients with critical coronary artery disease (CAD) was identified before. Adipose tissue functions as an endocrine organ and might contribute to an inflammatory burden which mediated by many adipokines in patients with CAD. In this study, we compare the expression of different inflammatory markers and adipokines in various origins of adipose tissues from CAD patient group and control group. Methods and Results—Samples of pericardial ,abdominal and subcutaneous adipose tissues were harvested at the outset of elective coronary artery bypass grafting(CABG) surgery (CAD group) and control group( including valve replacement surgery, patch repair of atrial septal defect and ventricular septal defect) (n=46v.s.12; age= 64±9 v.s.49±14 years). Local expression of adipokines (adiponectin, leptin, and visfatin,) and inflammatory cytokines [interleukin -6(IL-6), and tumor necrosis factor (TNF)-α] was analyzed by ELISA (protein release over 3 hours). Significantly higher levels of IL-6, TNF-α,leptin, and visfatin protein were observed in abdominal visceral adipose tissue, followed by pericardial and the lowest in subcutaneous adipose stores. Adiponectin has the opposite results. IL-6, TNF-α,leptin, and visfatin were significantly higher in any sort of adipose tissue in CAD group compared to the control group. Adiponectin also has the opposite effect, too. In CAD group, plasma leptin level of has stronger positive correlation with that of subcutaneous adipose tissue expression. In control group, plasma TNF-α level has stronger negative correlation with that of pericardial adipose tissue level. Conclusions—Abdominal visceral adipose tissue might play the most important role in atherosclerosis , insulin resistance and metabolic syndrome, followed by pericardial adipose tissue, and the least in subcutaneous adipose tissue.

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Coutu, Kevin. « Implication du tissu adipeux dans le développement de la prééclampsie et l’effet bénéfique de l’entrainement physique ». Thèse, 2019. http://hdl.handle.net/1866/22794.

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Ledoux, Sandra. « L'adiponectine stimule un patron génétique ovulatoire in vitro chez la truie ». Thèse, 2004. http://hdl.handle.net/1866/17478.

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