Relevant bibliographies by topics / Adiponectin/leptin

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Academic literature on the topic 'Adiponectin/leptin'

Author: Grafiati
Published: 2 June 2025
Last updated: 22 June 2025

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Journal articles on the topic "Adiponectin/leptin"

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Zhao, Shangang, Christine M. Kusminski, and Philipp E. Scherer. "Adiponectin, Leptin and Cardiovascular Disorders." Circulation Research 128, no. 1 (2021): 136–49. http://dx.doi.org/10.1161/circresaha.120.314458.

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The landmark discoveries of leptin and adiponectin firmly established adipose tissue as a sophisticated and highly active endocrine organ, opening a new era of investigating adipose-mediated tissue crosstalk. Both obesity-associated hyperleptinemia and hypoadiponectinemia are important biomarkers to predict cardiovascular outcomes, suggesting a crucial role for adiponectin and leptin in obesity-associated cardiovascular disorders. Normal physiological levels of adiponectin and leptin are indeed essential to maintain proper cardiovascular function. Insufficient adiponectin and leptin signaling results in cardiovascular dysfunction. However, a paradox of high levels of both leptin and adiponectin is emerging in the pathogenesis of cardiovascular disorders. Here, we (1) summarize the recent progress in the field of adiponectin and leptin and its association with cardiovascular disorders, (2) further discuss the underlying mechanisms for this new paradox of leptin and adiponectin action, and (3) explore the possible application of partial leptin reduction, in addition to increasing the adiponectin/leptin ratio as a means to prevent or reverse cardiovascular disorders.
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Bocian-Jastrzębska, Agnes, Anna Malczewska-Herman, Violetta Rosiek, and Beata Kos-Kudła. "Assessment of the Role of Leptin and Adiponectinas Biomarkers in Pancreatic Neuroendocrine Neoplasms." Cancers 15, no. 13 (2023): 3517. http://dx.doi.org/10.3390/cancers15133517.

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Data on the possible connection between circulating adipokines and PanNENs are limited. This novel study aimed to assess the serum levels of leptin and adiponectin and their ratio in patients with PanNENs and to evaluate the possible relationship between them and PanNEN’s grade or stage, including the presence of metastases. The study group consisted of PanNENs (n = 83), and healthy controls (n = 39). Leptin and adiponectin measurement by an ELISA assay was undertaken in the entire cohort. The serum concentration of adiponectin was significantly higher in the control group compared to the study group (p < 0.001). The concentration of leptin and adiponectin was significantly higher in females than in males (p < 0.01). Anincreased leptin–adiponectin ratio was observed in well-differentiated PanNENs (G1) vs. moderatelydifferentiated PanNENs (G2) (p < 0.05). An increased leptin–adiponectin ratio was found in PanNENs with Ki-67 < 3% vs. Ki-67 ≥ 3% (p < 0.05). PanNENs with distal disease presented lower leptin levels (p < 0.001) and a decreased leptin–adiponectin ratio (p < 0.01) compared with the localized disease group. Leptin, adiponectin, and the leptin–adiponectin ratio may serve as potential diagnostic, prognostic, and predictive biomarkers for PanNENs. Leptin levels and the leptin–adiponectin ratio may play an important role as predictors of malignancy and metastasis in PanNENs.
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Jardé, T., F. Caldefie-Chézet, N. Goncalves-Mendes, et al. "Involvement of adiponectin and leptin in breast cancer: clinical and in vitro studies." Endocrine-Related Cancer 16, no. 4 (2009): 1197–210. http://dx.doi.org/10.1677/erc-09-0043.

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Obesity is a risk factor for breast cancer development. A recent hypothesis suggests that the adipokines, adiponectin and leptin, are involved in breast cancer development. This prompted us to investigate the role of adiponectin and leptin in mammary carcinogenesis. Adiponectin receptors (AdipoR1 and AdipoR2) and leptin receptor (Ob-Rt, representing all the isoforms of Ob-R) proteins were detected by immunohistochemistry in in situ ductal carcinoma, invasive ductal malignancy, and healthy adjacent tissue. In addition, mRNA expression of adiponectin, AdipoR1, AdipoR2, leptin, Ob-Rt, and Ob-Rl (the long isoform of Ob-R) was observed in MCF-7 breast cancer cells. Interestingly, leptin mRNA expression was 34.7-fold higher than adiponectin mRNA expression in the MCF-7 cell line. Moreover, adiponectin (10 μg/ml) tended to decrease the mRNA expression of leptin (−36%) and Ob-Rl (−28%) and significantly decreased Ob-Rt mRNA level (−26%). In contrast, leptin treatment (1 μg/ml) significantly decreased AdipoR1 mRNA (−23%). Adiponectin treatment (10 μg/ml) inhibited the proliferation of MCF-7 cells, whereas leptin (1 μg/ml) stimulated the growth of cancer cells. In addition, adiponectin inhibited leptin-induced cell proliferation (both 1 μg/ml). Using microarray analysis, we found that adiponectin reduced the mRNA levels of genes involved in cell cycle regulation (mitogen-activated protein kinase 3 and ATM), apoptosis (BAG1, BAG3, and TP53), and potential diagnosis/prognosis markers (ACADS, CYP19A1, DEGS1, and EVL), whereas leptin induced progesterone receptor mRNA expression. In conclusion, the current study indicates an interaction of leptin- and adiponectin-signaling pathways in MCF-7 cancer cells whose proliferation is stimulated by leptin and suppressed by adiponectin.
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Mi, Jie, Mercedes Nancy Munkonda, Ming Li, et al. "Adiponectin and Leptin Metabolic Biomarkers in Chinese Children and Adolescents." Journal of Obesity 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/892081.

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Objective. To evaluate leptin and adiponectin as biomarkers of metabolic syndrome (MS) risk factors even in nonobese children/adolescents.Methods. Serum leptin, adiponectin, leptin:adiponectin ratio, lipids, glucose, and insulin concentrations as well as body size parameters and pubertal development were evaluated in a large population of Chinese children/adolescents (n=3505, 6–18 years, 1722 girls and 1783 boys).Results. Leptin concentration increased while adiponectin decreased with obesity, both were influenced by pubertal development. Central obesity had an additive effect on leptin levels (above obesity alone). Leptin/adiponectin increased 8.4-fold and 3.2-fold in overweight/obesity, and 15.8- and 4.5-fold with obesity plus MS, in early and late puberty, respectively. Even in normal weight children/adolescents, higher leptin and lower adiponectin concentrations associated with increased risk profile. Conversely, overweight/obese with lower leptin or higher adiponectin concentrations had a less compromised metabolic profile.Conclusion. Leptin, adiponectin, and leptin:adiponectin ratio are informative biomarkers for obesity, central obesity, MS, and abnormal metabolic profile even in normal weight children/adolescents.
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K, Selthofer-Relatić, Radić R, Stupin A, et al. "Leptin/adiponectin ratio in overweight patients – gender differences." Diabetes and Vascular Disease Research 15, no. 3 (2018): 260–62. http://dx.doi.org/10.1177/1479164117752491.

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Objective: Obesity-related atherosclerosis is a systemic disease with a background connected to multiple metabolic-neurohumoral pathways. The leptin/adiponectin ratio has been suggested as an atherosclerotic marker in obese patients. The aim of this study was to assess (1) the significance of the L/A ratio in overweight subjects, (2) the relation with anthropometric/metabolic parameters and (3) gender difference. Method: The study included 80 adult males and females, overweight, non-diabetic patients. Biochemical blood analysis and anthropometric and cardiovascular measurements were performed. Serum leptin levels were measured with a radioimmunoassay test and total adiponectin levels with enzyme-linked immunosorbent assay. Leptin/adiponectin ratios were calculated as ratios between total serum concentrations of leptin and adiponectin. Results: Differences between leptin, adiponectin serum levels and leptin/adiponectin ratios are presented in overweight persons, where females have a significantly higher leptin/adiponectin ratio than men ( p < 0.001). In men, the leptin/adiponectin ratio showed a positive correlation with total cholesterol levels ( p = 0.011), low-density lipoprotein ( p = 0.013) and triglycerides ( p = 0.032). In females, the leptin/adiponectin ratio correlated with anthropometric parameters of visceral obesity: waist circumference ( p = 0.001) and waist-to-hip ratio ( p = 0.025). Conclusion: The leptin/adiponectin ratio could represent an atherosclerotic risk marker of the early stage of obesity. Gender plays a significant role in pathophysiological changes, with different clinical manifestations, where sex hormones have a crucial effect on neurohumoral adipose tissue activity.
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Ambarwati, Ria, Damai Santosa, Eko Adhi Pangarsa, et al. "High Leptin and Low Adiponectin Levels in The Metabolic Syndrome Patients with Malignancy." Indonesian Biomedical Journal 15, no. 5 (2023): 297–303. http://dx.doi.org/10.18585/inabj.v15i5.2567.

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BACKGROUND: Metabolic syndrome (MetS), which is characterized by insulin resistance, adipocyte accumulation, and obesity, has been linked to malignancy development. Both leptin, an adipose tissue-produced cytokine-like hormone, and adiponectin, a hormone secreted by adipose tissue, play roles in the progression of MetS. However, the presence of leptin and adiponectin is also assumed to be associated with cancer proliferation. Therefore, it is necessary to investigate the profile of leptin and adiponectin levels in MetS patients with malignancy and non-malignancy.METHODS: This was a cross-sectional study involving 80 MetS subjects with and without malignancy. Leptin and adiponectin levels of subjects were analyzed by using the enzyme-linked immunosorbent assay (ELISA) method. Mann-Whitney tests were used to compare leptin and adiponectin levels between groups.RESULTS: Leptin levels were significantly higher in MetS patients with malignancy (32.99±22.47 ng/mL) than those without malignancy (6.17±7.46 ng/mL). Conversely, adiponectin levels were lower in the malignancy group (10.11±7.66 µg/mL) compared to the non-malignancy group (13.44±8.29 µg/mL), with both differences being statistically significant (p<0.001 for leptin, p=0.023 for adiponectin).CONCLUSION: Leptin levels were found to be higher while adiponectin levels were found to be lower in MetS patients with malignancy compared to those without malignancy. Therefore, it is suggested that leptin and adiponectin levels might be used as malignancy markers in MetS patients.KEYWORDS: adiponectin, leptin, metabolic syndrome, malignancy
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Mednova, Irina A., Anastasiia S. Boiko, Elena G. Kornetova, et al. "Adipocytokines and Metabolic Syndrome in Patients with Schizophrenia." Metabolites 10, no. 10 (2020): 410. http://dx.doi.org/10.3390/metabo10100410.

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The adipokines leptin, adiponectin, tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) might be associated with metabolic syndrome (MetS) in patients with schizophrenia. In the present study, we attempted to confirm the results of previous reports and assessed their MetS-related correlation with body fat composition and biochemical parameters. We measured in 46 patients with schizophrenia and MetS serum levels of adiponectin insulin, leptin, TNF-α and IL-6 and compared these levels to those of patients with schizophrenia without MetS. The MetS patients had significantly increased leptin levels and leptin/adiponectin ratios, as well as decreased adiponectin levels. Leptin levels correlated with several metabolic parameters, both in patients with and without MetS, including body fat percentage, total fat fold, and body mass index (BMI). Patients without abnormal MetS components had lower levels of leptin and leptin/adiponectin ratios compared with patients who had one or two MetS components. Leptin/adiponectin ratios were higher in patients who had four rather than three MetS components. Multiple regression analysis revealed multiple associations for leptin but only one for adiponectin, TNF-α, and IL-6. Our results support an important pathophysiological role for leptin more than adiponectin in patients with schizophrenia with MetS.
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Vega, Gloria Lena, and Scott M. Grundy. "Metabolic Risk Susceptibility in Men Is Partially Related to Adiponectin/Leptin Ratio." Journal of Obesity 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/409679.

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Background. High adiponectin/leptin ratio may be protective from metabolic risks imparted by high triglyceride, low HDL, and insulin resistance.Methods. This cross-sectional study examines plasma adipokine levels in 428 adult men who were subgrouped according to low (<6.5 μg/mL)and high (≥6.5 μg/mL)adiponectin levels or a low or high ratio of adiponectin/leptin.Results. Men with high adiponectin/leptin ratio had lower plasma triglyceride and higher HDL cholesterol than those with low ratio. Similarly, those with high adiponectin/leptin ratio had lower TG/HDL cholesterol ratio and HOMA2-IR than those with low ratio. In contrast, levels of adiponectin or the ratio of adiponectin/leptin did not associate with systolic blood pressure. But the ratio of adiponectin/leptin decreased progressively with the increase in the number of risk factors for metabolic syndrome.Conclusion. Adipokine levels may reflect adipose tissue triglyceride storage capacity and insulin sensitivity. Leptin is an index of fat mass, and adiponectin is a biomarker of triglyceride metabolism and insulin sensitivity. Men with high adiponectin/leptin ratios have better triglyceride profile and insulin sensitivity than men with a low ratio regardless of waist girth.
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Tonelli, Adriano R., Wassim H. Fares, Wael Dakkak, Youlan Rao, Xuan Zhou, and Raed A. Dweik. "Do single or sequential measurements of leptin and adiponectin in plasma have prognostic value in pulmonary arterial hypertension?" Pulmonary Circulation 7, no. 3 (2017): 727–29. http://dx.doi.org/10.1177/2045893217717219.

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Leptin (a neuroendocrine peptide that enhances metabolism and acts on the hypothalamus to suppress appetite) and adiponectin (a protein that has insulin-sensitizing, anti-inflammatory, and antiproliferative properties) are involved in the pathobiology of pulmonary arterial hypertension (PAH). We hypothesized that plasma leptin and adiponectin as well as the leptin/adiponectin ratio are abnormal in PAH patients and their levels track with disease severity and functional changes during follow-up. We tested this hypothesis in a cohort of patients included in the 16-week, international, multicenter, double-blind, placebo-controlled FREEDOM-C2 study. Blood was collected at baseline and week 16 in 178 out of 310 randomized patients with PAH. Baseline plasma leptin and adiponectin concentrations were 25 ± 31 ng/mL and 7.8 ± 6.1 ug/mL, respectively. Leptin, adiponectin, and leptin/adiponectin (mean ± SD) changes at 16 week were of small magnitude. Leptin at baseline was significantly associated with older age, higher BMI, higher Borg dyspnea index, and lower NT-pro BNP. Women had higher levels of leptin than men (30.5 ± 33.2 versus 7.2 ± 6.4 ng/mL), even when adjusting for background therapy and etiology (linear regression: β = 21.8, P < 0.001). Adiponectin was negatively associated with BMI and positively associated with NT-pro BNP. Changes in leptin, adiponectin, and leptin/adiponectin ratio adjusted for weight at 16 weeks did not predict functional class, distance walk in 6 min or survival at one, two, three, or four years. Plasma leptin and adiponectin at baseline and their change at 16-week do not appear to significantly impact prognosis in PAH.
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Matovic, Sara, Christoph Rummel, Elena Neumann, Jennifer McGrath, and Jean-Philippe Gouin. "Adverse Childhood Experiences Influence Longitudinal Changes in Leptin But Not Adiponectin." Biopsychosocial Science and Medicine 87, no. 2 (2025): 118–28. https://doi.org/10.1097/psy.0000000000001366.

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Objective Adverse childhood experiences (ACEs) are associated with a greater risk of obesity and cardiometabolic disease. Adipokines, including leptin and adiponectin, play vital roles in biological processes linked to obesity and cardiometabolic risk. The adiponectin/leptin ratio may represent a marker of impaired hormonal regulation of adipose tissue. Prior cross-sectional studies suggest patterns of higher plasma leptin and lower adiponectin among adults who have experienced ACEs. This study addresses whether ACEs influence longitudinal changes in leptin, adiponectin, and the adiponectin/leptin ratio, after accounting for current chronic stress and adiposity. Methods This longitudinal study included 192 middle-aged mothers (mean age = 46.78 years) experiencing higher (n = 108) and lower (n = 84) chronic caregiving stress. Adipokines and adiposity were measured at three timepoints: T1 (baseline), T2 (15 months later), and T3 (30 months after T1). ACEs were assessed retrospectively using the Childhood Trauma Questionnaire. Results Mixed-effect models showed that leptin and adiponectin increased over time. Greater ACEs exposure was associated with larger increases in leptin over time, but it was not related to adiponectin or the adiponectin/leptin ratio. Current caregiving stress was not related to leptin and adiponectin levels and did not interact with ACEs in predicting adipokine levels. Mediation analyses revealed that increases in waist circumference partially mediated the association between ACEs and increases in leptin over time. Conclusions ACEs may increase vulnerability to cardiometabolic risk in midlife caregiving mothers through its influence on longitudinal changes in leptin and central adiposity.
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Dissertations / Theses on the topic "Adiponectin/leptin"

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Ahire, Shwetal. "Maternal adiposity and plasma concentrations of leptin and adiponectin." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1250701408.

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Ahire, Shwetal V. "Maternal adiposity and the plasma concentration of leptin and adiponectin." Cincinnati, Ohio : University of Cincinnati, 2009. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1250701408.

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Thesis (M.S.)--University of Cincinnati, 2009.<br>Advisor: Debra Krummel. Title from electronic thesis title page (viewed Oct. 20, 2009). Includes abstract. Keywords: pregnancy; skinfold; leptin; adiponectin; obesity. Includes bibliographical references.
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McMath, Arden Lee. "Associations Between Physical Activity Level and Adiponectin/Leptin Ratios in Older Adults." Miami University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=miami1556816283317575.

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Rausch, Jamie Ann. "Secondary Data Analysis Investigating Effects of Marine Omega-3 Fatty Acidson Circulating Levels of Leptin and Adiponectin in Older Adultswith Chronic Venous Leg Ulcers." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu158652907707218.

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Pratap, Anishchal Anshil. "Analysis of adiponectin, leptin and their receptor expression in the 5XFAD mouse model of Alzheimer’s disease." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24135.

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Alzheimer’s disease (AD) is a neurodegenerative disorder that primarily affects individuals over 65 years of age. Pathological hallmarks of the disease include amyloid plaques and neurofibrillary tangles. Individuals with metabolic syndromes such as obesity and type-2 diabetes share similar pathologies with AD patients including insulin resistance, cortical atrophy and neuroinflammation. Adipocyte-derived leptin and adiponectin regulates metabolism, energy expenditure and satiety via their receptors, LepR, AdipoR1 and AdipoR2, respectively. Impaired leptin and adiponectin signalling causes metabolic dysregulation in obesity and diabetes. To determine the role of metabolic dysregulation in the AD brain, this thesis focusses on the expression profiles of leptin and adiponectin receptors and their relationship with neuroinflammation in the brain of the 5XFAD mouse model of AD. Expression of AdipoR1 and AdipoR2 in the brains of 5XFAD mice at advanced stages of the disease was investigated in chapter two. Utilizing immunofluorescent staining, neuronal expression of AdipoR1 and AdipoR2 was significantly reduced and robust expression of AdipoR2 by reactive astrocytes was observed in 5XFAD mice compared to age-matched controls. AdipoR2-expressing astrocytes were also observed in regions regulating metabolism, including the dorsomedial hypothalamic and thalamic paraventricular nuclei in the 5XFAD brain. Increased inflammation surrounding metabolic centres and decreased neuronal AdipoR1 and AdipoR2 suggests metabolic disturbance in 5XFAD mice. Leptin expression in the 5XFAD brain was investigated in chapter three. Analysis utilizing immunofluorescent staining on 5XFAD mice at early and late stages of AD revealed an age-related perturbation of neuronal leptin and LepR expression. Astrocytic expression of leptin and LepR was robust in aged 5XFAD mice and accompanied increased plaque loading and neuroinflammation, compared to younger 5XFAD animals. The shift in LepR, AdipoR1 and AdipoR2 expression from neurons to astrocytes in aged 5XFAD mice suggests that astrocytes may utilize leptin and adiponectin signalling to mediate their reactive state to degrade amyloid in the AD brain. Taken together, these findings provide evidence of impaired leptin and adiponectin signalling in the AD brain.
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Barsnick, Rosa. "Hormones of Energy Metabolism in Critically Ill Foals: Insulin, Glucagon, Leptin, Adiponectin, Ghrelin and Growth Hormone." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1275523617.

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Jacobson, Sofie. "Severe sepsis : epidemiology and sex-related differences in inflammatory markers." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96214.

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Background.  Sepsis is a syndrome associated with high mortality rates, substantial morbidity and high costs of care. The incidents of sepsis is reported to be high and controversy exists whether gender affect severity or outcome. Little is known about factors determining suscepti­bility for developing the syndrome and severity of the syndrome once developed. Early detection and adequate antibiotic administration are the mainstay of treatment and means to identify patients with particular high risk of adverse outcome are desirable. There are data to suggest that the course of sepsis and outcome from the syndrome may be influenced by inherited differences in the immunological response among humans Aims: Paper I: Assess incidence and outcome for ICU-treated sepsis patients in this region; Paper II: Assess if there are gender differences related to characteristics, aspects of treatment or out­come in sepsis in this region. Paper III: Assess the association of baseline levels of leptin and adiponectin and future sepsis event, and association of these adipokines in the cute phase and sepsis severity and outcome. Paper IV: Assess association of baseline levels of mannose-binding lectin (MBL) and future sepsis event, and MBL levels in the acute phase in relation to sepsis severity and outcome. Results. Paper I:  Overall ICU mortality rate was 25%, while the ICU mortality for patients with septic shock was 58% in this retrospective single university hospital cohort analysis. Cardio­vascular disease and diabetes were the most prevalent comorbidities among patients who died during hospital stay.  Paper II:  No gender-related differences in mortality or length of stay was found in this prospective single center observational study. Differences in aspects of treatment were related to differences in site of infection. Men had more often infections in skin and skin-structures, whereas women more often had abdominal infections. Early organ dysfunction asses­sed as SOFA score at admission was a stronger predictor for hospital mortality for women than for men. The discrepancy was related to the SOFA coagulation-sub score.  Paper III: In this nes­ted case-referent study hyperleptinemia at baseline predicted a first-ever sepsis event, even after adjustment for BMI and other cardiovascular risk factors. Hyperleptinemia in the acute sepsis phase was associated with reduced risk of in-hospital death in men, but associated with increased risk of in-hospital   death in women.  Paper IV: In the same matched cohort as in Paper III high baseline levels of MBL predicted a first ever sepsis event. High MBL levels in the acute phase or an increase from baseline to the acute phase associate with increased in-hospital death in women but not in men. Low MBL levels was not identified as a risk for acute sepsis or in-hospital death. Conclusions. Mortality from severe sepsis is high, equally affecting men and women. There are differences in patient characteristics and inflammatory markers, which associate with in-hospital mortality differentially in men and women. Aspects of gender should be mandatory, and genetic analysis are desired in future sepsis research.
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Dinca, Madalina, Maria-Corina Serban, Amirhossein Sahebkar, et al. "Does vitamin D supplementation alter plasma adipokines concentrations? A systematic review and meta-analysis of randomized controlled trials." Elsevier B.V, 2016. http://hdl.handle.net/10757/605887.

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We aimed to elucidate the role of vitamin D supplementation on adipokines through a systematic review and a meta-analysis of randomized placebo-controlled trials (RCTs). The search included PUBMED, Scopus, Web of Science and Google Scholar through July 1st, 2015. Finally we identified 9 RCTs and 484 participants. Meta-analysis of data from 7 studies did not find a significant change in plasma adiponectin concentrations following vitamin D supplementation (mean difference [MD]: 4.45%, 95%CI: -3.04, 11.93, p=0.244; Q=2.18, I(2)=0%). In meta-regression, changes in plasma adiponectin concentrations following vitamin D supplementation were found to be independent of treatment duration (slope: 0.25; 95%CI: -0.69, 1.19; p=0.603) and changes in serum 25-hydroxy vitamin D [25(OH)D] levels (slope: -0.02; 95%CI: -0.15, 0.12; p=0.780). Meta-analysis of data from 6 studies did not find a significant change in plasma leptin concentrations following vitamin D supplementation (MD: -4.51%, 95%CI: -25.13, 16.11, p=0.668; Q=6.41, I(2)=21.97%). Sensitivity analysis showed that this effect size is sensitive to one of the studies; removing it resulted in a significant reduction in plasma leptin levels (MD: -12.81%, 95%CI: -24.33, -1.30, p=0.029). In meta-regression, changes in plasma leptin concentrations following vitamin D supplementation were found to be independent of treatment duration (slope: -1.93; 95%CI: -4.08, 0.23; p=0.080). However, changes in serum 25(OH)D were found to be significantly associated with changes in plasma leptin levels following vitamin D supplementation (slope: 1.05; 95%CI: 0.08, 2.02; p=0.033). In conclusion, current data did not indicate a significant effect of vitamin D supplementation on adiponectin and leptin levels.<br>Revisión por pares
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Nickisch, Sabine. "Glukosetoleranz 24 Stunden postpartal und deren Beziehung zu anthropometrischen Daten sowie Adipozytokinserumkonzentrationen." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-101180.

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Während der Schwangerschaft vollziehen sich im Körper der Frau verschiedene Adaptionsmechanismen, um eine bestmögliche Versorgung für das heranwachsende Kind zu gewährleisten. Bei fortschreitender Gravidität entwickelt sich eine physiologische Insulinresistenz. Gelingt es den maternalen Betazellen des Pankreas‘ nicht, diese zu kompensieren, kann eine diabetische Stoffwechsellage bis hin zur Ausbildung eines Gestationsdiabetes (GDM) entstehen. Adipozytokine beeinflussen direkt lokale und periphere metabolische, endokrinologische sowie immunologische Prozesse. Inwieweit sie in der Gravidität eine Rolle spielen, ist bislang nicht hinreichend geklärt. In verschiedenen Studien wurde eine Beziehung zwischen den Fettgewebshormonen und der Glukosetoleranz in der Schwangerschaft nachgewiesen. Im Rahmen dieser Dissertation sollte eine Analyse zur Glukosetoleranz und zu Adipozytokinserumspiegeln bei Frauen unmittelbar nach der Entbindung vorgenommen werden. Ergebnisse oraler Glukosetoleranztests von gesunden Frauen 24 Stunden postpartal (n=65) wurden mit denen einer nicht-schwangeren, gesunden Kohorte (n=30) verglichen. Maternale und neonatale anthropometrische Daten wurden in Zusammenhang zu Adipozytokinen gestellt. Im Vergleich zu Frauen mit normaler Glukosetoleranz (NGT) postpartal konnten in dieser Studie signifikant verminderte Blutglukose – sowie nüchtern – Proinsulinspiegel in der nicht-schwangeren Kontrollgruppe nachgewiesen werden, wohingegen die nüchtern-C-Peptidspiegel erhöht waren. Weiterhin zeigten sich postpartal signifikant niedrigere Adiponektin-, aber höhere sOB-R- (soluble leptin receptor) sowie Leptinspiegel der NGT-Mütter im Vergleich zur Kontrollgruppe. Zusätzlich konnte eine Beziehung zwischen Adipozytokinserumspiegeln und Parametern der Glukosetoleranz bzw. Adipositas demonstriert werden. Daraus lässt sich die These ableiten, dass Frauen in der frühen Phase nach der Entbindung ähnliche biochemische Konstellationen wie beim metabolischen Syndrom, der gestörten Glukosetoleranz oder bei Störungen des Adipozytokinsystems aufweisen.
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Will, Katja [Verfasser]. "Untersuchungen zum Einfluss der Adipokine Adiponectin und Leptin auf das Wachstum porciner Skelettmuskelzellen in vitro / Katja Will." Greifswald : Universitätsbibliothek Greifswald, 2014. http://d-nb.info/1053684789/34.

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Books on the topic "Adiponectin/leptin"

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Neumann, Elena, Klaus Frommer, and Ulf Müller-Ladner. Acute-phase responses and adipocytokines. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0058.

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Adipokines, also called adipocytokines, are highly bioactive substances mainly expressed by adipose tissue. In addition to adipocytes, different cell types resident in various tissues produce adipokines under pathophysiological conditions. Adipokines include a growing number of pluripotent molecules such as adiponectin, resistin, leptin, and visfatin. Since distinct effects of adipokines on inflammation have been described, their influence on the (innate) immune system has been investigated in rheumatology, gastroenterology, and endocrinology. This review gives an overview on the current knowledge about the influence which adipokines have on the immune system and chronic inflammation in rheumatic diseases.
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Book chapters on the topic "Adiponectin/leptin"

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Engin, Atilla. "Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-63657-8_15.

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Laron, Zvi, and Hannah Kanety. "Adiponectin and Leptin in Laron Syndrome." In Laron Syndrome - From Man to Mouse. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11183-9_16.

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Yu, Jerry Zhong, Kamyar Kalantar-Zadeh, and Connie M. Rhee. "Adiponectin and Leptin in Kidney Disease Patients." In Endocrine Disorders in Kidney Disease. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-97765-2_20.

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Brakenhielm, Ebba, and Yihai Cao. "Leptin, Adiponectin, and Other Adipokines in Regulation of Adipose Tissue Angiogenesis." In Angiogenesis in Adipose Tissue. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8069-3_10.

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Fantuzzi, Giamila. "Adipokines: Leptin and Adiponectin in the Regulation of Inflammatory and Immune Responses." In Adipose Tissue and Adipokines in Health and Disease. Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9_6.

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Lenz, Anne M., and Frank Diamond. "The Importance of the Adiponectin and Leptin Relationship in In Utero and Infant Growth." In Handbook of Growth and Growth Monitoring in Health and Disease. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_169.

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Bronsky, J., and K. Mitrova. "Adiponectin, adipocyte fatty acid-binding protein and leptin in human breast milk and impact in the infant." In Handbook of dietary and nutritional aspects of human breast milk. Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-764-6_21.

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Tu, Hong. "Leptin/Adiponectin." In Handbook of Biologically Active Peptides. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-385095-9.00072-5.

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Gavrila, A., D. Barb, and C. S. Mantzoros. "Leptin, Adiponectin, Resistin, Ghrelin." In Encyclopedia of Stress. Elsevier, 2007. http://dx.doi.org/10.1016/b978-012373947-6.00543-2.

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GAVRILA, A., D. BARB, and C. MANTZOROS. "Leptin, Adiponectin, Resistin, Ghrelin." In Encyclopedia of Stress. Elsevier, 2007. http://dx.doi.org/10.1016/b978-012373947-6/00543-2.

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Conference papers on the topic "Adiponectin/leptin"

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Nicolaou, N., J. Joseph, and I. N. Bruce. "AB0277 Leptin and adiponectin levels in rheumatoid arthritis patients." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.1189.

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Kryfti, Maria, Vasilis Galenterides, Katerina Dimakou, Michail Toumbis, and Gourgoulianis Konstantinos. "Effects of smoking cessation on serum leptin and adiponectin levels." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1883.

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Jeong, Y.-J., H.-Y. Jeong, J.-G. Bong, S.-H. Park, J.-H. Choi, and H.-K. Oh. "P4-09-17: Leptin and Adiponectin Expression in Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-09-17.

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Andersson, Lars I., Anna James, Barbro Dahlen, Sven-Erik Dahlen, Apostolos Bossios, and On Behalf Of Bioair Consortium. "Oral steroids induce leptin and adiponectin in subjects with airway obstructive diseases." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3346.

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Oliveira, E. S., F. M. Kattah, N. Figueiredo, et al. "Association of Adiponectin, Leptin, and Daytime Sleepiness in Women with Severe Obesity." In XIX Congresso Brasileiro do Sono. Thieme Revinter Publicações Ltda., 2023. http://dx.doi.org/10.1055/s-0043-1770259.

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Yabushita, Hiromitsu, Keita Iwasaki, Taiki Ueno, and Akihiko Wakatsuki. "Abstract 4738: Clinicopathological roles of adiponectin receptor and leptin receptor in endometrial carcinoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4738.

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Azrad, Maria, Barbara A. Gower, Gary R. Hunter, and Tim R. Nagy. "Abstract B81: Racial differences in serum adiponectin and leptin before and after weight loss." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-b81.

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Howell, DL, NL Lugogo, S. Degan, et al. "Leptin Levels and Adiponectin Receptor Expression Are Increased in the Airways of Obese Asthmatics." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2515.

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Galiutina, O., S. Shevchuk, Y. Seheda, and I. Kuvikova. "AB0130 Serum leptin and adiponectin levels in rheumatoid arthritis patients, their association with inflammatory process." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5343.

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Ashktorab, Hassan, Akbar Soleimani, Alexandra Nichols та ін. "Abstract 3130: Adiponectin, Leptin, IGF1 and TNFα serum biomarker as noninvasive diagnosis of colon adenoma". У Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3130.

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Reports on the topic "Adiponectin/leptin"

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Yuan, Qihang. Association of circulating leptin level, adiponectin level and risk of pancreatic cancer: a combination of traditional and dose-response meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.4.0138.

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