Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9BY76 (adipokine)
 3,147 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adipose tissue produces and secretes multiple adipokines. Most studies on adipokine production/expression have been performed on whole adipose tissue. In addition, data concerning an overall of adipokine expression are scarce and can be heterogeneous depending on the obesity model studied. Our first aim was to compare the expression of adipokines involved in the interplay between obesity and insulin resistance in isolated adipocytes from different mouse models of obesity displaying different levels of weight gain and insulin sensitivity. The second aim was to determine perigonadal/subcutaneous ratio of each adipokine. Only resistin expression was decreased in obese mice without modifications in glucose and insulin blood levels. In addition to decreased levels of resistin, obesity models associated with hyperglycemia and hyperinsulinemia presented an increased expression of leptin and tumor necrosis factor-alpha (TNFalpha). Obese and diabetic mice were the only animals to exhibit high expression of plasminogen activator inhibitor type-1 and interleukin-6. All adipokines except TNFalpha were more heavily expressed in perigonadal than in subcutaneous adipocytes. Interestingly, fat-enriched diet and overweight on their own did not modify the distribution of adipokines between the two fat depots. However, severe obesity modified the distribution of proinflammatory adipokines. In conclusion, the level and number of adipokines with altered expression increased with obesity and hyperinsulinemia in mice. The physiopathological impact of depot-specific differences of adipokine expression in adipocytes remains to be clarified.
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PMID:Adipokine expression profile in adipocytes of different mouse models of obesity. 1637 31

Compensatory beta cell growth occurs in accordance to overweight and increasing insulin demands. The proliferative actions of insulin and insulin-like growth factors are mediated via the IRS-2-PI(3)K-Akt pathway of pleiotropic insulin signaling. However, sustained activation leads to negative feedback via the mTOR-induced proteasomal degradation of IRS-2. The proliferative actions of incretins and adipokines are mediated via other pathways that ultimately converge with the IRS-2-PI(3)K-Akt axis. The incretins GIP and GLP-1 increase IRS-2 levels in beta cells by acting via the cAMP-PKA pathway, whereas leptin inhibits PTEN activity via CK2-dependent pathways. By increasing PIP(3) availability the adipokine amplifies the magnitude as well as duration of factors acting via the IRS-2-PI(3)K-Akt pathway. Considering that AMPK prevents mTOR-induced degradation of IRS-2, we propose that adiponectin and leptin cooperatively achieve compensatory beta cell growth in accordance to adiposity. In conditions of overt obesity, when adiponectin levels are too low to provide sufficient IRS-2 levels, loss of compensatory beta cell growth may occur.
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PMID:Leptin and adiponectin regulate compensatory beta cell growth in accordance to overweight. 1709 72

The aim of the present study was to examine the effect of exercise training on adipokines, inflammatory markers, and oxidative stress in overweight children. Nineteen overweight children were randomly assigned to an aerobic exercise training or sedentary control group for 8 weeks. Measurements included peak oxygen uptake (V o(2)max), body weight and composition, adipokines (C-reactive protein, interleukin 6, tumor necrosis factor alpha, adiponectin, leptin, and resistin), and oxidative stress (8-isoprostane). There were no differences between groups for change in body weight or composition over the 8 weeks. Exercise training improved V o(2)max (exercise group, 1.64 +/- 0.13 to 1.85 +/- 0.17L/min vs control group, 1.83 +/- 0.12 to 1.60 +/- 0.13 L/min, P < .05) but did not change any of the measured adipokines or the marker of systemic oxidative stress, 8-isoprostane. These data suggest that in the absence of weight loss, exercise training alone does not improve the adipokine profile or levels of oxidative stress in overweight children.
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PMID:In the absence of weight loss, exercise training does not improve adipokines or oxidative stress in overweight children. 1757 Feb 65

We examined the relationships between plasma vitamin C, adiposity, and the collagen-like adipokine, adiponectin. Of 118 sedentary, nonsmoking adults participating in the cross-sectional trial (35 men and 83 women aged 38.7 +/- 1.0 y with BMI of 30.4 +/- 0.6 kg/m2, plasma vitamin C concentrations of 43.5 +/- 1.3 micromol/L, and plasma adiponectin concentrations of 8.9 +/- 0.3 mg/L), 54% were obese and 24% were overweight. Plasma vitamin C was inversely related to BMI, percentage of body fat, and waist circumference in both women and men (r = -0.383 to -0.497, P < 0.025). In women but not men, these associations remained significant after controlling for body mass. Plasma vitamin C was directly related to plasma adiponectin in the women after controlling for age and vitamin C supplement use (r = 0.222, P = 0.049) but not after controlling for body mass. Twenty obese men and women participated in an intervention trial and consumed an energy-restricted diet low in vitamin C (approximately 38 mg/d) for 8 wk. Subjects were stratified by age, gender, and BMI and randomly assigned to receive placebo or vitamin C (500 mg) capsules daily. At baseline, plasma adiponectin was directly related to plasma vitamin C (r = 0.609, P = 0.021) and inversely related to body mass (r = -0.785, P = 0.001). Body mass decreased significantly during the 8 wk study in both the vitamin C (n = 6, -5.9 +/- 0.9 kg) and placebo groups (n = 8, -6.5 +/- 0.7 kg). Plasma adiponectin increased 13% from baseline by wk 8 in both groups (P < 0.05). In summary, plasma vitamin C was inversely related to markers of adiposity, particularly in women, but vitamin C supplementation did not influence the circulating concentration of adiponectin.
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PMID:Plasma vitamin C is inversely related to body mass index and waist circumference but not to plasma adiponectin in nonsmoking adults. 1758 27

Thirty-four children were assessed for body composition, blood pressure, lipids, glucose tolerance, markers of insulin resistance, oxidative stress, and adipokines. Children were divided into 3 groups: (1) normal weight, (2) overweight but otherwise healthy, and (3) overweight with the metabolic syndrome. There were no differences among any of the groups for age or Tanner stage, and anthropometric variables were similar between the overweight and the overweight with the metabolic syndrome groups. Differences across groups were found for high-density lipoprotein cholesterol (P < .001), triglycerides (P < .01), fasting insulin (P < .001), homeostasis model assessment (P < .01), adiponectin (P < .05), leptin (P < .0001), C-reactive protein (P < .0001), interleukin 6 (P < .0001), and 8-isoprostane (P < .001). In children, oxidative stress and adipokine levels worsen throughout the continuum of obesity and especially in the presence of components of the metabolic syndrome. Overweight children with components of the metabolic syndrome may be at elevated risk for future cardiovascular disease.
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PMID:Oxidative stress and adverse adipokine profile characterize the metabolic syndrome in children. 1767 10

Obesity is a major global health problem and is associated with low-grade inflammation and, in a number of cases, poor iron status. We speculated that the adipokine leptin might play a role in regulating iron metabolism in the overweight population because it shares a number of common biological features with IL-6, a major factor in the development of the anemia of chronic disease via its stimulatory actions on the production and release of the iron regulatory hormone hepcidin. To test this hypothesis, we exposed HuH7 human hepatoma cells to leptin and measured hepcidin mRNA expression by quantitative PCR. HuH7 cells were also transfected with a hepcidin promoter-luciferase reporter gene construct to investigate transcriptional regulation of hepcidin. In leptin-treated cells, hepcidin mRNA expression was enhanced significantly. Preincubation with a Janus kinase (JAK) 2 inhibitor significantly diminished this response. Hepcidin promoter activity was also increased in the presence of leptin. This effect was decreased either by mutation of the signal transducer and activator of transcription (STAT) 3 binding motif in the hepcidin promoter or by coexpressing a dominant-negative STAT3 mutant. These data suggest that leptin upregulates hepatic hepcidin expression through the JAK2/STAT3 signaling pathway. As a consequence, the increased production of leptin in overweight individuals might be a major contributor to the aberrant iron status observed in these population groups.
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PMID:Leptin increases the expression of the iron regulatory hormone hepcidin in HuH7 human hepatoma cells. 1795 71

Visfatin, is a new adipokine, highly expressed in the visceral fat of both mice and humans. To examine whether visfatin is expressed in human peripheral monocyte-enriched mononuclear cells and whether its expression is altered in type 2 diabetes (DM2), we compared 24 DM2 women [17 overweight (BMI >25) and 7 lean (BMI<25)] to 26 healthy women (14 overweight and 12 lean), all premenopausal. Relative visfatin mRNA levels were significantly higher (approximately 3-fold) in DM2 compared to healthy control women (p<0.02), independently of the presence of overweight/obesity. Mononuclear TNF-alpha and IL-6 mRNA expression was also elevated in DM2 compared to control women (p=0.001 and p=0.004, respectively), an increase observed in both lean and overweight DM2 women. By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). Circulating visfatin and TNF-alpha levels did not differ either between the lean and the overweight subgroups of DM2 and control women, while IL-6 plasma levels were significantly higher in both overweight subgroups compared to their lean counterparts. In conclusion, visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes, independent of their BMI, which may enhance the effects of their adipose-derived levels and may contribute to the increased insulin resistance and atherogenic risk of these patients.
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PMID:Visfatin, TNF-alpha and IL-6 mRNA expression is increased in mononuclear cells from type 2 diabetic women. 1795 40

One mechanism by which breast-feeding may protect against the development of childhood obesity is through the activity of components of breast milk. In an article published in this issue of Epidemiology, Weyermann et al found that overweight at age 2 years was associated with higher levels of adiponectin, a hormone secreted by fat cells, in the breast milk of mothers who breast-fed their infants for at least 6 months. This finding is surprising for several reasons: it is doubtful that infants absorb ingested adiponectin; prior literature suggests that adiponectin would reduce, rather than increase, risk for overweight; and the authors did not find associations with breast milk leptin, another adipokine. It is possible that adipokine exposure in infancy determines later weight status, but fundamental research is needed on associations of circulating adipokines with excess weight gain and on determinants of adipokine levels.
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PMID:Breast-feeding, adipokines, and childhood obesity. 1804 87

The abundance of the adiponectin receptors, AdipoR1 and AdipoR2, and the effects of the antidiabetic adipokine adiponectin in monocytes of normal-weight and overweight controls and type 2 diabetic patients (T2D) were analyzed. AdipoR1 and AdipoR2 mRNAs were increased in monocytes of obese controls and T2D patients when compared to normal-weight controls, and AdipoR1 mRNA positively correlated to AdipoR2 mRNA, the waist to hip ratio and systemic adiponectin. However, AdipoR1 and AdipoR2 proteins were lower in monocytes of T2D compared to normal-weight donors. Induction of IL-6 and IL-8 by adiponectin, an effect involving p38 MAPK, was also reduced in T2D monocytes.
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PMID:Reduced response to adiponectin and lower abundance of adiponectin receptor proteins in type 2 diabetic monocytes. 1844 81

Adiponectin is an adipocyte-derived protein with atheroprotective and immunoregulatory function. Adiponectin and activin A reduce foam cell formation and adiponectin activates the p38 MAPK pathway that is well described to induce activin A. Therefore, it was analyzed whether adiponectin alters activin A in primary human monocytes. Adiponectin dose- and time-dependently induced activin A in the supernatant, and the maximal amount was observed after 12h of incubation. Adiponectin-stimulated release of activin A was blocked by a p38 MAPK inhibitor. Metformin and pioglitazone are drugs frequently used to treat diabetic patients and metformin slightly reduced monocytic activin A release whereas pioglitazone had no effect. Type 2 diabetes is associated with elevated inflammatory systemic cytokines but activin A serum levels were similar in slim probands, overweight controls and type 2 diabetic patients. Furthermore, activin A did not correlate to systemic adiponectin, body mass index, waist to hip ratio or C-reactive protein. These findings indicate that adiponectin upregulates monocytic activin A release via the p38 MAPK pathway, and this may in part explain the immunoregulatory and antiatherosclerotic effects of this adipokine.
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PMID:Adiponectin upregulates monocytic activin A but systemic levels are not altered in obesity or type 2 diabetes. 1912 83


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