JAK-STATs通路及肥胖发病机制探究进展.docVIP

JAK/STATs通路及肥胖发病机制探究进展周增丁1综述，李小林2 巫国辉2审校 [摘要]瘦素(leptin)是一种由肥胖基因(obese gene，ob基因)编码、由白色脂肪组织合成和分泌的蛋白质，与肥胖的发病密切相关。leptin主要通过Janus激酶/信号转导及转录激活子通路(Janus kinase/signal transducer and activator of transcription pathway，JAK/STATs通路)参与体脂代谢、机体摄食，能够有效抑制肥胖的产生。然而近来研究发现在肥胖个体中普遍存在着leptin抵抗、血液中高leptin表达；leptin并不能发挥体脂调控作用。其失活机制还不是十分清楚，研究表明JAK/STATs通路异常与机体内leptin失活存在密切关系。本文就肥胖与JAK/STATs通路的关系进行综述。 [关键词]leptin；leptin抵抗；肥胖；JAK/STATs通路 [中图分类号]Q813.1[文献标识码]A [文章编号]1008-6455（2009）02-0271-04 Progress on JAK/STATs pathway and pathogenesis of obesity ZHOU Zeng-ding1,LI Xiao-lin2,WU Guo-hui2 (1. Medical college of nanchang university,Nanchang 330006,Jiangxi,China;2.Department of Plastic and maxillofacial Surgery, Jiangxi Provincial People’s Hospital, Nanchang 330006, Jiangxi, China) Abstract：Leptin is a protein encoded by obese gene(ob gene),mainly synthesised and secreted by white adipose tissue,and it is closely related to the incidence of obesity.Primarily using the Janus kinase /signal transducer and activator of transcription pathway(JAK/STATs pathway)to involve in fat metabolismfood intake and can effectively suppress the emergence of obesity. However, recent study found that obese individuals are in the prevalence of leptin resistance and high blood leptin expression;leptin does not play a role in regulating body fat.The mechanism is not very clear, some studies showed that it was a close relationship between JAK/STATs pathway abnormal and leptininactivation.This article on obesity caused by leptin resistence and JAK/STATs pathway relations were reviewed. Key words: leptin;leptin resistence;obesity;JAK/STATs pathway 进入新世纪以来，肥胖年轻化趋势越来越明显，研究已经证实肥胖会提高心脑血管疾病、糖尿病等的发病率和死亡率[1]。了解肥胖的发病机理以及如何有效的控制肥胖的产生成为当前刻不容缓需要解决的问题。leptin的发现开创了肥胖认识和控制的新纪元；十几年来，人们对leptin以及leptin抵抗、JAK/STATs通道的认识不断深入，为肥胖研究及临床防治指明了崭新方向。 1leptin 1.1 leptin结构、分泌及表达调控：leptin是由ob基因编码的一种分子量为16KD的分泌型蛋白质,由167个氨基酸残基组成。其主要由白色脂肪组织合成和分泌。leptin分泌具有节律变化，在午夜和凌晨最高，中午至下午最低，但肥胖者昼间leptin变化较弱而且搏动衰弱。在分泌入血过程中，去除了其中由