Editorial
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Apr 7, 2009; 15(13): 1537-1547
Published online Apr 7, 2009. doi: 10.3748/wjg.15.1537
Hepatitis C virus and type 2 diabetes
Francesco Negro, Mahnaz Alaei
Francesco Negro, Mahnaz Alaei, Division of Gastroenterology, Hepatology and Clinical Pathology, University Hospitals, 24 rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
Francesco Negro, Division of Clinical Pathology, University Hospitals, 24 rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
Author contributions: Negro F conceived and wrote the manuscript; Alaei M did a literature search and participated in the writing of the manuscript; both authors approved its final version.
Correspondence to: Francesco Negro, MD, Associate Professor, Division of Gastroenterology, Hepatology and Clinical Pathology, University Hospitals, 24 rue Micheli-du-Crest, 1211 Geneva 14, Switzerland. francesco.negro@hcuge.ch
Telephone: +41-22-3795800  
Fax: +41-22-3729366
Received: December 18, 2008
Revised: January 21, 2009
Accepted: January 28, 2009
Published online: April 7, 2009
Abstract

This review focuses on the relationship between hepatitis C virus (HCV) infection and glucose metabolism derangements. Cross-sectional and longitudinal studies have shown that the chronic HCV infection is associated with an increased risk of developing insulin resistance (IR) and type 2 diabetes (T2D). The direct effect of HCV on the insulin signaling has been analyzed in experimental models. Although currently available data should be considered as preliminary, HCV seems to affect glucose metabolism via mechanisms that involve cellular pathways that have been implicated in the host innate immune response. IR and T2D not only accelerate the histological and clinical progression of chronic hepatitis C, but also reduce the early and sustained virological response to interferon-alpha-based therapy. Thus, a detailed knowledge of the mechanisms underlying the HCV-associated glucose metabolism derangements is warranted, in order to improve the clinical management of chronic hepatitis C patients.

Keywords: Hepatitis C; Fibrosis; Insulin resistance; Insulin signaling; Type 2 diabetes