Polycystic ovary syndrome (PCOS) is a heterogeneous, multi-causal, and genetically complex disorder, which is related to the failure in endocrine glands. Adiponectin has been reported to be low in PCOS, even in the absence of adiposity. Quercetin reduces serum glucose, insulin, triglycerides, and cholesterol levels and increases the expression and secretion of adiponectin. The aim of this study was to determine the effect of quercetin on the adiponectin-mediated insulin sensitivity in PCOS patients. Eighty-four women with PCOS were selected and randomly assigned to 2 groups of treatment and control. The treatment group received 1 g quercetin (two 500 mg capsules) daily for 12 weeks, and the control group received placebo. In addition to anthropometric assessments, fasting serum levels of total adiponectin, high-molecular-weight (HMW) adiponectin, glucose, insulin, testosterone, LH, and SHBG were also measured at the baseline and at the end of the trial. Quercetin could slightly increase the level of adiponectin by 5.56% as compared to placebo (adjusted p-value=0.001) and HMW adiponectin by 3.9% as compared to placebo (adjusted p-value=0.017), while it reduced the level of testosterone (0.71 ng/dl in quercetin vs. 0.77 ng/dl in placebo; p<0.001) and LH (8.42 IU/l in quercetin vs. 8.68 IU/l in placebo; p=0.009). HOMA-IR levels were also significantly (p<0.001) lower in quercetin (1.84) group compared to placebo group (2.21). Oral quercetin supplementation was effective in improving the adiponectin-mediated insulin resistance and hormonal profile of women with PCOS.

Plasma visfatin concentrations are lower in patients with GDM and related to glycemic control reflected by HbA1c. Furthermore, visfatin does not seem to be correlated with dietary intake in pregnant women.

BackgroundDiabetes refers to a group of metabolic diseases with blood glucose of higher than normal ranges. Furthermore, n-3 polyunsaturated fatty acids are necessary for the regulation of the activity of human function. The effect of n-3 PUFA on diabetes has been investigated in animal studies, yet, the exact amount has not been set, to date. Irisin, as a new myokine, is released from skeletal muscle and Irisin levels decrease as a result of physical inactivity, overweightness, and obesity. Also, the reduction of serum irisin level is associated with development of insulin resistance and type 2 diabetes. This study was performed to assess the effects of n-3 PUFA supplementation on serum irisin level in patients with diabetes.MethodsThis randomized clinical trial included 43 patients with type 2 diabetes (21 patients in the placebo group and 22 patients in the n-3 PUFA supplement group). They were randomized to groups, one receiving 10 weeks of either n-3 PUFA supplement and the other the placebo (1250 mg capsule, three times per day). Samples were also matched by age, gender, and body mass index (BMI) in the 2 groups. Anthropometric measurements, demographic information and dietary intakes were obtained both before and after the intervention. Serum irisin levels were measured before and after the intervention using human irisin enzyme linked immunosorbent assay (ELISA) kit. Independent t-test was used to compare the mean outcomes between groups.ResultsAt baseline, irisin serum levels were not significantly different between the placebo and n-3 PUFA supplementation groups (P > 0.05). However, a significant change was observed between the groups after intervention (P = 0.04). Also there was a significant difference in mean change (after versus before the intervention) (P = 0.05). Compared to the placebo, n-3 PUFA supplementation decreased serum FBS and HbA1C (P = 0.036 and 0.001; respectively). Also, there were significant differences between changes of diastolic blood pressure and HOMA-IR after the intervention between the groups. The duration of illness was not considered as a confounding factor because there was no significant association between irisin level (after versus before the intervention) and the illness duration.ConclusionsThe current study indicated that n-3 PUFA supplementation with a dosage of 1250 mg three times per day, resulted in increased serum irisin level of diabetic patients.

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The aim of the present study was to compare the levels of visfatin in portal and systemic circulations and to assess the possible relationship of visfatin with systemic inflammation and insulin resistance in morbidly obese patients undergoing bariatric surgery. A total of 46 morbidly obese patients (BMI = 45.3 ± 5.3 kg/m(2)) undergoing bariatric surgery were included in this study. Blood samplings were performed simultaneously from portal and systemic veins during surgery. Visfatin was measured in both portal and systemic venous samples. Besides, fasting serum levels of insulin, glucose, lipid profile, visfatin, and hs-CRP were determined in systemic venous blood samples. Insulin sensitivity was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR). Visfatin concentrations were significantly higher in portal vein than systemic veins (11.9 ± 12.1 vs. 5.1 ± 3.3 ng/ml, p < 0.0001). While systemic levels of visfatin were significantly correlated with circulating levels of hs-CRP (r = 0.527, p < 0.0001), there were no significant correlations between portal levels of visfatin with systemic levels of hs-CRP concentrations. Substantially higher levels of visfatin in portal vein than systemic veins provide evidence that visceral adipose tissue is the major secretory source of visfatin in humans. Our findings underscore that visceral adipose tissue is an active endocrine organ that is involved in the complex interrelationship between obesity and pathologic conditions.