Peer-review started: June 8, 2014
First decision: July 10, 2014
Revised: July 20, 2014
Accepted: November 17, 2014
Article in press: November 19, 2014
Published online: January 27, 2015
Processing time: 219 Days and 1.2 Hours
Hepatic steatosis is commonly seen in the patients with chronic hepatitis C virus (HCV) infection. HCV is closely associated with lipid metabolism, and viral steatosis is more common in genotype 3 infection owing to a direct cytopathic effect of HCV core protein. In non-genotype 3 infection, hepatic steatosis is considered largely to be the result of the alterations in host metabolism; metabolic steatosis is primarily linked with HCV genotype 1. Adipose tissue secretes different hormones involved in glucose and lipid metabolisms. It has been demonstrated that adipocytokines are involved in the pathogenesis of non-alcoholic fatty liver disease, as the decreased plasma adiponectin levels, a soluble matrix protein expressed by adipoctyes and hepatocyte, are associated with liver steatosis. Various studies have shown that steatosis is strongly correlated negatively with adiponectin in the patients with HCV infection. The role of adiponectin in hepatitis C virus induced steatosis is still not completely understood, but the relationship between adiponectin low levels and liver steatosis is probably due to the ability of adiponectin to protect hepatocytes from triglyceride accumulation by increasing β-oxidation of free fatty acid and thus decreasing de novo free fatty acid production.
Core tip: Three main types of steatosis in the patients with hepatitis C virus (HCV) infection are known: a metabolic type associated with metabolic syndrome, viral steatosis directly triggered by the virus and a “middle ground” between metabolic and viral mechanisms. Liver steatosis is a common histological feature of chronic hepatitis C infection, and the recent studies have shown that it is strongly correlated negatively with adiponectin levels. This finding suggests that adiponectin may have a role in modulating the progression of hepatic steatosis in HCV infected patients.