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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。
Leptin, a protein encoded by the obese gene (ob gene) and synthesized and secreted by white adipose tissue, is closely related to the pathogenesis of obesity. Leptin is involved in the metabolism of body fat mainly through the Janus kinase / signal transducer and activator of transcription pathway (JAK / STATs pathway), which can effectively inhibit the production of obesity. However, recent studies have found that leptin resistance is generally present in obese individuals and that high leptin is expressed in the blood; leptin does not exert the effect of body fat regulation. The mechanism of its inactivation is not yet clear, studies have shown that abnormal JAK / STATs pathway and in vivo leptin inactivation are closely related. This article reviews the relationship between obesity and JAK / STATs pathways.