Role of insulin resistance and hepatic steatosis in the progression of fibrosis and response to treatment in hepatitis C
Article first published online: 4 JAN 2011
© 2011 John Wiley & Sons A/S
Special Issue: Proceedings of the 4th Paris Hepatitis Conference. The publication of this supplement was supported by an unrestricted educational grant from F. Hoffmann-Laroche Ltd.
Volume 31, Issue Supplement s1, pages 23–28, January 2011
How to Cite
Sanyal, A. J. (2011), Role of insulin resistance and hepatic steatosis in the progression of fibrosis and response to treatment in hepatitis C. Liver International, 31: 23–28. doi: 10.1111/j.1478-3231.2010.02397.x
- Issue published online: 4 JAN 2011
- Article first published online: 4 JAN 2011
- Received 10 November 2010Accepted 3 December 2010
- chronic hepatitis C;
- insulin resistance;
- metabolic syndrome;
- non-alcoholic steatohepatitis;
Hepatitis C is a common cause of chronic viral infection of the liver. It is associated with insulin resistance and the development of type 2 diabetes mellitus. It is also associated with the development of hepatic steatosis. The presence of hepatic steatosis is associated with an increased risk of having hepatic fibrosis. This is also associated with the severity of insulin resistance. These findings are specifically germane for those with genotype1 infection. Genotype 3 infection independently causes steatosis and successful treatment of the virus is followed by resolution of steatosis. In genotype 1 infection, the presence of hepatic steatosis is also a risk factor for failure to respond to pegylated interferon and ribavirin therapy. Unfortunately efforts to treat insulin resistance prior to antiviral therapy have not been very successful. Newer efforts focused on the role of specific micro RNAs in mediating the metabolic effects of hepatitis C virus infection may provide to ameliorate the metabolic risks of HCV infection.