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Hepatitis C virus (HCV) is a major cause of progressive liver damage, infecting an estimated 3% of the world population. Morbidity and mortality associated with chronic hepatitis C are mainly attributable to progression towards cirrhosis and its end-stage complications. Thus, the main goal of treatment is the prevention of liver disease progression, an objective that can be attained via the eradication of HCV infection with antiviral therapy. The current standard of care consists of a combination of pegylated interferon α (IFNα) and ribavirin, with a cure rate of about 55%. Novel effective direct antiviral agents (DAA), targeting specific viral functions, are expected to be commercially available towards the end of 2011, raising hopes of significant improvements in the cure rates.
An important aspect of HCV infection is its idiosyncratic relationship with the metabolism of glucose,1 which negatively affects liver disease progression and the response to IFNα-based therapies1 while also raising the possibility of multifaceted and clinically relevant interactions with the metabolic syndrome. Although many viral infections induce insulin resistance, the effect of HCV on glucose metabolism is remarkable and supported by a large amount of clinical, epidemiological and experimental data.1 Changes in glucose metabolism are more significant in patients …