肝脏胰岛素抵抗与2型糖尿病  

Hepatic Insulin Resistance and Type 2 Diabetes Mellitus

作　　者：刘福君 常李李 王为兰[1] 李金耀[1] LIU Fujun;CHANG Lili;WANG Weilan;LI Jinyao(Xinjiang Key Laboratory of Biological Resources and Genetic Engineering,College of Life Science and Technology,Xinjiang University,Urumqi 830046,China)

机构地区：[1]新疆大学生命科学与技术学院新疆生物资源基因工程重点实验室,乌鲁木齐830046

出　　处：《中国医学科学院学报》2022年第4期699-708,共10页Acta Academiae Medicinae Sinicae

基　　金：新疆维吾尔自治区自然科学青年基金(2020D01C070);新疆维吾尔自治区重点实验室开放课题(2021D04019)。

摘　　要：胰岛素抵抗(insulin resistance, IR)是因肝脏等靶组织对胰岛素敏感下降导致高胰岛素血症、糖耐量受损的一种病理性反应。IR作为2型糖尿病典型的病理特征,其发病机制是抗糖尿病研究的焦点。本文就糖尿病状态下的糖代谢、脂代谢、氧化应激、线粒体功能障碍、内质网应激、炎症与肝脏胰岛素抵抗相关信号通路的分子生物学机制进行综述,为糖尿病治疗提供新思路及理论指导。Insulin resistance(IR) is a pathological reaction of hyperinsulinemia and impaired glucose tolerance caused by decreased sensitivity of target tissues such as liver to insulin.The pathogenesis of IR as a typical pathological feature of type 2 diabetes is the focus of anti-diabetes research.In this paper, we reviewed the molecular mechanisms of glucose and lipid metabolism, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and hepatic IR in the case of type 2 diabetes mellitus, which might provide new ideas and theoretical guidance for the treatment of diabetes mellitus.

关 键 词：糖尿病 肝脏 胰岛素抵抗 信号通路 作用机制 

分 类 号：R34[医药卫生—基础医学]