炎症和自噬及其交互作用在胰岛素抵抗中作用机制的研究进展

doi:10.13481/j.1671-587x.20190348

摘要/Abstract

摘要： 胰岛素抵抗是2型糖尿病的早期症状、核心特征和主要发病机制之一。胰岛素抵抗是机体对正常剂量胰岛素的生理性应答减弱，导致机体葡萄糖摄取和利用效率下降，因此为维持机体血糖的稳定，保证正常生理功能，机体自发代偿性地分泌过多胰岛素从而产生高胰岛素血症。引起胰岛素抵抗的主要原因为各种刺激导致的胰岛素转导信号通路异常。由肥胖引起的慢性炎症状态和自噬被证实在胰岛素抵抗的发生发展中起重要作用，炎症信号通路的激活及炎症因子的大量释放干扰胰岛素受体信号转导，自噬失调可导致内质网应激和线粒体功能紊乱等，从而影响胰岛素信号通路，导致胰岛素抵抗。炎症和自噬在胰岛素不同靶器官中的作用机制各不相同，慢性炎症状态和自噬可相互影响、相互调节，共同在胰岛素抵抗中发挥作用，使胰岛素抵抗的发生机制更为复杂。本文就慢性炎症状态和自噬在胰岛素不同靶器官中的作用机制及二者的交互作用进行综述。

关键词: 炎症反应, 自噬, 胰岛素抵抗, 交互作用, 内质网应激, 2型糖尿病

中图分类号:

R335.6

杨丽娜, 曹媛. 炎症和自噬及其交互作用在胰岛素抵抗中作用机制的研究进展[J]. 吉林大学学报(医学版), 2019, 45(03): 742-746.

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