Since the identification of hepatitis C virus (HCV) in the late 1980s, chronic HCV infection has emerged as a complex multifaceted disease with manifestations extending beyond the liver. As such, hepatic steatosis, insulin resistance (IR), and type II diabetes have been observed to occur more frequently in association with HCV infection than other chronic inflammatory liver disease.¹ A proportion of HCV infected patients with steatosis also exhibit several of the clinical features seen in non-alcoholic steatohepatitis (NASH), questioning the significance of these metabolic disorders in the pathogenesis of HCV related liver disease. Hence, considerable HCV research has recently been directed towards understanding the mechanisms underlying the development of these metabolic manifestations in HCV infected patients and their implications in the progression of liver disease. Several important questions have been examined: are these metabolic disorders in HCV infected patients a result of viral or host factors and, if viral, how do viral proteins interfere with lipid and insulin metabolism? What is the primary event in these patients (steatosis or IR) and what are the implications of steatosis and IR in the pathogenesis of liver disease? Finally, how can we exploit our current knowledge for developing effective therapeutic strategies for HCV infected patients?

In this issue of Gut, Fartoux and colleagues² utilise the homeostasis model assessment for IR (HOMA IR) index to study the association between steatosis and IR in patients with chronic HCV infection (see page 1003). In order to examine this association, the authors excluded patients with alternate factors known to be associated with the development of steatosis (such as alcohol intake >20 …