The role of circulating miRNAs in leptin resistance in obese children

Emre Murat Altınkılıç, Selami Bayrakdar, Gülcan Seymen Karabulut, B. Haliloglu, R. Attar
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引用次数: 3

Abstract

Abstract Objectives Leptin resistance is one of the important causes of obesity in children. Besides known causes of leptin resistance like mutations in leptin and leptin receptor genes, overexpression of SOCS3 in arcuate nucleus is a potential cause of leptin resistance. We aimed to determine the effects of circulating miRNAs on leptin resistance in obese children by targeting SOCS3 pathway. Methods miRNAs potentially targeting SOCS3 were determined by using online target prediction databases. Polymorphisms in miRNA target sequences were determined by using online genome browsers. miRNA expression levels of obese (n=35) and non-obese (n=30) children were determined by qPCR method, genotyping were performed by real-time PCR method and serum leptin, leptin receptor and SOCS3 levels were measured by ELISA method. Results miRNA profiling have shown that serum miR-218-5p levels are significantly (p<0.05) increased in accordance with serum leptin levels in obese children. Conclusions In this study we used target prediction methods for evaluating potential miRNAs which may involve in development of leptin resistance. We have shown that miR-218-5p might be taking part in leptin resistance in obese children.
循环mirna在肥胖儿童瘦素抵抗中的作用
目的瘦素抵抗是儿童肥胖的重要原因之一。除了已知的瘦素抵抗的原因,如瘦素和瘦素受体基因的突变,弓形核中SOCS3的过度表达是瘦素抵抗的潜在原因。我们旨在通过靶向SOCS3途径确定循环mirna对肥胖儿童瘦素抵抗的影响。方法利用在线靶标预测数据库确定潜在靶向SOCS3的mirna。利用在线基因组浏览器确定miRNA靶序列的多态性。采用qPCR法检测肥胖儿童(n=35)和非肥胖儿童(n=30)的miRNA表达水平,采用实时荧光定量PCR法进行基因分型,ELISA法检测血清瘦素、瘦素受体和SOCS3水平。结果miRNA分析显示,肥胖儿童血清miR-218-5p水平与血清瘦素水平同步显著升高(p<0.05)。在本研究中,我们使用了靶标预测方法来评估可能参与瘦素抵抗发展的潜在mirna。我们已经证明miR-218-5p可能参与肥胖儿童瘦素抵抗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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