HCV感染与IR相关关系的研究进展  

The Research Progress of Relationship between HCV Infection and Insulin Resistance

作　　者：郑增光 何琼琼[1] 王颖[1] 杨晓静[1] 冯德云[1] 

机构地区：[1]中南大学基础医学院病理学系,湖南长沙410013 [2]浙江省肿瘤医院病理科,浙江杭州310022

出　　处：《现代生物医学进展》2016年第1期179-183,共5页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(81270501)

摘　　要：丙型肝炎是丙型肝炎病毒(HCV)感染以肝组织损伤为主的全身感染性疾病。HCV感染者中胰岛素抵抗(IR)和高胰岛素血症的高发比率已引起国内外学者广泛重视;对其的研究也日益深入,胰岛素抵抗不仅可以加速肝脏损伤的进程,而且影响抗病毒治疗的疗效;此外,尚可增加2型糖尿病、脂肪肝、动脉粥样硬化等代谢性疾病的患病机会。HCV通过多条途径干预胰岛素的信号传导,包括增加炎性细胞因子如肿瘤坏死因子-a(TNF-a)的分泌、胰岛素受体底物-1的磷酸化和以其糖异生基因如葡萄糖6磷酸酶、磷酸烯醇式丙酮酸羧激酶2的上调。本文将主要就HCV病毒干扰胰岛素信号传导通路而导致胰岛素抵抗的发生机制,以及期望通过对胰岛素抵抗机制的研究,研制出逆转胰岛素抵抗的靶向药物。Hepatitis c is a infectious diseases caused by hepatitis c virus, which mainly lead to the damage of liver tissue and cells. Scholars from home and abroad are interested in the high incidence rates of Insulin resistance（IR） and Hyperinsulinemia; Insulin resistance can not only accelerate the process of the injury of hepatic cell, but also influence the curative effect of antiviral therapy; Various mechanisms have been proposed in regard to HCV mediated insulin resistance, involving up regulation of inflammatory cytokines,like tumor necrosis factor-α, phosphorylation of insulin-receptor substrate-1, up-regulation of gluconeogenic genes like glucose 6 phosphatase, phosphoenolpyruvate carboxykinase 2. In this review, we mainly summarize the available information on how HCV infection interferes with insulin signaling pathways resulting in insulin resistance and expect targeted drugs to reverse insulin resistance.

关 键 词：HCV 胰岛素抵抗 发生机制 疗效 

分 类 号：R512.63[医药卫生—内科学]