ABSTRACT
Objective: polycystic ovary syndrome [PCOS], an ovarian-pituitary axis androgen disorder, is a common endocrine disease in women. Obesity-induced androgenesis and imbalance of adipokine secretion may lead to some metabolic features of PCOS. The beneficial effects of polyphenolic compounds such as quercetin have been reported, however, the underlying molecular mechanism is not entirely understood. In the present study, we investigated the effect of quercetin supplementation on the expression of adiponectin receptors at the transcript level in peripheral blood mononuclear cells [PBMC] samples of PCOS patients
Materials and Methods: in this randomized clinical trial, 84 PCOS subjects were randomly assigned to two groups; the treatment group received 1 g quercetin [two 500 mg capsules] daily for 12 weeks and the control group received placebo. To examine the effect of quercetin supplementation on PCOS patients in addition to biochemical and anthropometric assessments, the expression of ADIPOR1 and ADIPOR2 at the transcript level and AMPK level were determined by quantitative reverse transcription-polymerase chain reaction [RT-qPCR] and ELISA assays respectively
Results: oral quercetin supplementation significantly increased ADIPOR1 and ADIPOR2 transcript expression by 1.32- and 1.46-fold respecetively [P<0.01]. In addition, quercetin supplementation enhanced AMPK level by 12.3% compared with the control group [P<0.05]
Conclusion: oral quercetin supplementation improves the metabolic features of PCOS patients by upregulating the expression of adiponectin receptors and AMPK [Registration Number: IRCT2013112515536N1]
ABSTRACT
Objective: Jo determine the effect of supplementation with n-3 polyunsaturated fatty acids (PUFAs) on circulatory resis-tin and monocyte chemoattractant protein 1 [MCP-1] levels in type 2 diabetes mellitus [T2DM] patients
Subjects and Methods: This was a 10-week, placebo-controlled, double-blind, randomized trial of n-3 PUFAs [2,700 mg/day] versus placebo [soft gels containing 900 mg of edible paraffin]. Forty-four T2DM patients were supplemented with n-3 PUFAs and another 44 patients received placebo (3 patients discontinued the trial]. Serum resistin, MCP-1, and the lipid profile were measured before and after supplementation. The adi-ponectin-resistin index [1 + Iog[10] [resistin] - Iog10 [adiponec-tin]] and atherogenic index [Iog[10] triglyceride/high-density lipoprotein cholesterol] of plasma [an indicator of cardiovascular complications] were assessed. The independent Student t test was used to assess the differences between the supplement and placebo groups and the paired f test to analyze the before/after changes
Results: In this study, n-3 PUFAs reduced serum MCP-1 levels [from 260.5 to 230.5 pg/ ml_;p = 0.002], but they remained unchanged in the placebo group, n-3 PUFAs could not decrease serum resistin levels. The adiponectin-resistin index was significantly reduced after supplementation with n-3 PUFAs when compared to theplacebo. The atherogenic index was also significantly improved after supplementation with n-3 PUFAs [from 1.459 to 1.412; p = 0.006]
Conclusions: The MCP-1 levels and lipid profile were improved after supplementation with n-3 PUFAs, but resistin serum levels were not changed. Hence, the anti-inflammatory effects of n-3 PUFAs might be mediated by targeting MCP-1
ABSTRACT
Visfatin, a novel adiopocytokine, has been proven to be a proinflammatory mediator involved in the process of atherosclerosis. Visfatin has been shown to play a role in plaque destabilization as it is found abundantly in foam cell macrophages within unstable atherosclerotic plaques. The present study is designed to investigate the potential association between serum vistafin levels and the risk of acute myocardial infarction [AMI]. There were 72 patients [mean age: 61.57 +/- 11.40 years] as cases who presented with first-time AMI that were assessed 8 hours after the incident. The control group consisted of 83 healthy volunteers [mean age: 60.30 +/- 8.32 years]. Plasma visfatin levels were measured using enzyme immunoassay in both groups. Biochemical parameters were analyzed. Blood pressure, body mass index [BMI], waist circumference, diabetes, and hypertension were recorded. Serum visfatin levels were significantly higher in patients with AMI [12.77 +/- 8.06 ng/ml] compared to controls [6.57 +/- 2.96 ng/ml, P 7.244 ng/ml [log visfatin > 0.86] had a sensitivity of 70% and a specificity of 75% for predicting AMI. We have detected high levels of visfatin in patients with AMI. It can be concluded that proinflammatory cytokines such as visfatin may play a role in the development of atherosclerosis as well as destabilization of the atherosclerotic plaque