Department of Pathology and Immunology, Centre Médical Universitaire, Rue Michel-Servet 1, Geneva, Switzerland.
Expert Rev Gastroenterol Hepatol. 2011 Aug;5(4):503-16. doi: 10.1586/egh.11.43.
Important breakthroughs have been made in recent years into understanding the close interaction between hepatitis C virus (HCV) infection and glucose homeostasis. Both cross-sectional and longitudinal studies have demonstrated that infection with HCV is associated with an increased risk of developing insulin resistance and Type 2 diabetes. A direct effect of HCV on hepatocyte insulin signaling has been shown in experimental models. Some preliminary observations seem to suggest that indirect mechanisms involving extrahepatic organs might also play a role. The interaction between HCV and glucose metabolism has significant clinical consequences. Insulin resistance and Type 2 diabetes not only accelerate the histological and clinical progression of chronic hepatitis C, but also reduce the virological response to IFN-α-based therapy. Thus, understanding the mechanisms underlying HCV-associated glucose metabolism derangements is of paramount interest in order to improve the clinical management of chronic hepatitis C. This article will focus on the studies that consistently argue in favor of an interrelation between HCV and insulin resistance and will highlight the latest discoveries in this field.
近年来，人们在理解丙型肝炎病毒 (HCV) 感染与葡萄糖稳态之间的密切相互作用方面取得了重要突破。横断面和纵向研究都表明，HCV 感染与胰岛素抵抗和 2 型糖尿病的发病风险增加有关。实验模型表明，HCV 对肝细胞胰岛素信号有直接影响。一些初步观察结果似乎表明，涉及肝外器官的间接机制也可能发挥作用。HCV 与糖代谢之间的相互作用具有重要的临床后果。胰岛素抵抗和 2 型糖尿病不仅加速慢性丙型肝炎的组织学和临床进展，而且降低了基于 IFN-α的治疗的病毒学反应。因此，了解 HCV 相关糖代谢紊乱的机制对于改善慢性丙型肝炎的临床管理至关重要。本文将重点介绍那些一致认为 HCV 与胰岛素抵抗之间存在关联的研究，并强调该领域的最新发现。
