Oral quercetin supplementation enhances adiponectin receptor transcript expression in polycystic ovary syndrome patients: a randomized placebo-controlled double-blind clinical trial

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]

Vitamin D Binding Protein as screening biomarker candidate for late-onset preeclampsia without intrauterine growth restriction during 16 week of gestation

The aim of this investigation was conducted to proteomic analysis of plasma obtained from pregnant women who destined to develop late-onset preeclampsia without intrauterine growth restriction [IUGR] during 16[th] week of gestation. Plasma was obtained from primiparous women during 16[th] week of gestation. 2-DE proteomic analysis was done for plasma from 11 healthy pregnant women and 11 women who developed preeclampsia later. Using bioinformatic analysis with Progenesis SameSpots ver4.0 software and ANOVA test, expression of 2 spots were statistically different between two groups. In preeclamptic state, expression of both were decreased, one of these spots was vitamin D binding protein [p-value: 0.047], the other one will be discussed in another paper. According to results, we concluded that during 16[th] week of gestation, occurance of late-onset preeclampsia without IUGR is predictable. During this week, pathology of disease is present and may be the process of placental degeneration and impaired placentation are include in disease pathology

[Ceramide can induce leukocyte common antigen-related [lar] gene at mrna and protein level in c2c12 muscle cells]

Type 2 diabetes results from two defects, insulin resistance and beta cell dysfunction. At the molecular and cellular levels, there is a connection between fatty acid accumulation and insulin resistance in muscles. Although several mechanisms involved in FFA-induced muscle insulin resistance, the exact mechanism is poorly understood. Recent studies show that the defect in insulin signaling pathway might be underlying mechanism for FFA-induced insulin resistance in the muscle. Protein tyrosine phosphatases like Leukocyte common antigen-related [LAR] are the key elements of insulin signaling and they can be a candidate in FFA induced insulin resistance. Studies have shown that type 2 diabetes involved and obese individuals have had increased levels of LAR in their tissues. However, the responsible factor for LAR overexpression is not well understood. In this study we investigate ceramide effect on LAR expression in the muscle cells. In this laboratory study C2C12 cells [mouse skeletal] after differentiation to myotubes using 2% of horse serum for 4 days, treated with 50 and 100 mMs of C2ceramide for 16h. RNA extracted, cDNA synthesized and Real Time PCR using specific primers for LAR and beta actin used. To detect LAR protein levels western blot was used. 100 mMs Ceramide [45%, P<0.01] significantly induced LAR mRNA expression but there was not significant difference between 50mM ceramide and untreated cells. The results from real time confirmed by protein data. 100 mMs Ceramide [52%, P<0.01] significantly induced LAR protein levels in comparison of control. The data from this study provide evidence that ceramide around pathologic concentration induce LAR expression. Results supported by human studies that were showed that diabetic and obese persons have a high level of LAR expression and revealed ceramide can be one of the responsible factors for inducing LAR expression in diabetic patients. However, further investigations are needed to clarify exact role of LAR in FFA induced insulin resistance.