丙型肝炎病毒相关胰岛素抵抗的机制。

Mechanisms of hepatitis C virus-related insulin resistance.

机构信息

Departments of Internal Medicine and Pathology and Immunology, Divisions of Gastroenterology and hepatology and of Clinical pathology, University Hospitals, University of Geneva Medical Center, 1, rue Michel-Servet, 1205 Geneva, Switzerland.

出版信息

Clin Res Hepatol Gastroenterol. 2011 May;35(5):358-63. doi: 10.1016/j.clinre.2011.01.011. Epub 2011 Feb 25.

DOI:10.1016/j.clinre.2011.01.011

PMID:21354385

Abstract

The hepatitis C virus (HCV) infection has been shown to have direct and/or indirect effects on glucose metabolism, leading to insulin resistance and, in predisposed individuals, type 2 diabetes. This is supported by several experimental, clinical and epidemiological data. The detailed molecular events leading to insulin resistance in HCV-infected patients are unclear. HCV infects primarily the liver and, to a very minor extent, mononuclear cells. Direct interactions between HCV products and the hepatocyte insulin signaling pathway have been reported by several authors. However, recent evidence supports the existence of a significant extrahepatic component of HCV-induced insulin resistance. Thus, the molecular pathogenesis of glucose metabolism disturbances observed in hepatitis C is much more complex than expected. The clinical management of such condition remains empirical.

摘要

丙型肝炎病毒（HCV）感染已被证明对葡萄糖代谢有直接和/或间接的影响，导致胰岛素抵抗，在易感个体中则导致 2 型糖尿病。这得到了几项实验、临床和流行病学数据的支持。导致 HCV 感染患者胰岛素抵抗的详细分子事件尚不清楚。HCV 主要感染肝脏，其次是单核细胞。一些作者报道了 HCV 产物与肝细胞胰岛素信号通路之间的直接相互作用。然而，最近的证据支持 HCV 诱导的胰岛素抵抗存在显著的肝外成分。因此，丙型肝炎患者观察到的葡萄糖代谢紊乱的分子发病机制比预期的要复杂得多。这种情况的临床管理仍然是经验性的。