胰岛素抵抗的分子学机制  

Molecular Mechanism of Insulin Resistance

作　　者：李影[1] 闫鹏[1] 董平栓[1] 

机构地区：[1]河南科技大学第一附属医院心血管内科,河南洛阳471003

出　　处：《医学综述》2014年第17期3122-3124,共3页Medical Recapitulate

摘　　要：胰岛素受体底物(IRS)丝氨酸磷酸化是胰岛素信号转导通路中的一种时间依赖性生理反馈机制,代谢及炎症应激阻断其磷酸化进而导致胰岛素抵抗。诱导胰岛素抵抗的因素激活了包括抑制性κB激酶(IKKβ)、c-Jun氨基端激酶(JNK)、细胞外信号调节激酶、雷帕霉素靶蛋白通路和p70S6激酶在内的激酶,进而导致失控的IRS丝氨酸磷酸化。因此,这些激酶是抗胰岛素抵抗的潜在药物靶点,IKKβ/核因子κB或JNK通路靶向治疗未来可能发展为糖尿病治疗方法。Insulin receptor substrates （IRS） serine phosphorylation is a time-controlled physiological feedback mechanism in the insulin signal transduction pathway that is blocked by metabolic and inflammatory stresses to promote insulin resistance. Kinases,including IKK~, JNK, ERK, roTOR, and S6K, activated by the factors that induce the insulin resistance lead to the serine phosphorylation of uncontrolled IRS. Therefore, those kinases are the potential drug targets against insulin resistance and the targeting of IKKβ/NF-κB or .INK oathwav mac be develoned as the treatment for diabetes in future.

关 键 词：胰岛素 胰岛素抵抗 2型糖尿病 分子生物学 

分 类 号：R34[医药卫生—基础医学]