ECE2017 Guided Posters Obesity (12 abstracts)
1Department of Biochemistry, Faculty of Medicine, Iran University of Meical Sciences, Tehran, Iran; 2Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran; 3H.Aliasghar Hospital, Iran University of Medical Sciences, Tehran, Iran; 4Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Obesity is one of the major causes of morbidity and mortality worldwide and is considered a risk factor for metabolic syndrome, type 2 diabetes and cardiovascular disease (CVD). miRNAs are epigenetic regulators of several aspects of metabolism and energy homeostasis and are involved in obesity and regulation of insulin sensitivity. miR 26b is among the obesity-related micoRNAs and is differentially expressed in preadipocytes and mature adipocytes in humans and is upregulated during adipocyte maturation. Visfatin which is implicated in insulin resistance and metabolic syndrome is a target of miR-26b. The aim of this study was to investigate the levels of miR-26b levels in obesity and its association with insulin resistance and metabolic parameters.
Methods: Seventy children and adolescents (35 controls; 35 obese), between the ages of 8 and 18 years, were selected and clinically evaluated. The expression of miR-26b was measured after microRNA extraction from plasma samples. The extracted microRNAs were elongated using poly A polymerase reaction followed by cDNA synthesis. Real-time PCR was performed using SYBR green and delta Ct was calculated by the formula: Ct (reference gene)-Ct (target gene). miR-16 was used as the reference gene. Insulin and visfatin levels were measured using ELISA, and insulin resistance was calculated by the homeostasis model of assessment of insulin resistance (HOMA-IR). Fasting plasma glucose, triglyceride, total cholesterol, LDL-C and HDL-C were also measured colorimetrically.
Results: miR-26b expression were significantly lower in obese subjects compared with control group and were also lower in subjects with insulin resistance compared to those without insulin resistance. miR-26b was significantly correlated with insulin levels and HOMA-IR. It also showed a significant negative correlation with visfatin which was higher in obese subjects compared with control subjects.
Conclusion: Decreased miR-26b expression in obese children and adolescents may be involved in insulin resistance and increased visfatin levels.