| [ Summary ] |
Although the primary target of hepatitis C viral (HCV) infection is the liver, it has become increasingly evident that HCV can induce diseases in numerous organs. Recently, a great deal of attention has been drawn to metabolic disorders in relation to HCV infection. Initially, hepatic steatosis and disturbances in lipid metabolism have been found to be characteristic of HCV infection. A correlation has also been noted between HCV infection and diabetes. It is now evident that HCV by itself can induce insulin resistance by way of disturbing the intracellular signaling pathways of insulin through the function of HCV core proteins. Insulin resistance, caused by HCV infection, evolves into type 2 diabetes in relation to high-fat diets and obesity. The fact that HCV infection induces insulin resistance through the virus itself may influence our view of the progression of chronic hepatitis and create novel therapeutic approaches. Some metabolic aspects of hepatitis C resemble NASH in numerous ways such as the presence of steatosis, serum dyslipidemia, and overproduction of oxidative stress in the liver, warranting the designation of hepatitis C as a steatohepatitis. In contrast, there are noticeable differences, between hepatitis C and NASH, in that HCV modulates cellular gene expression and intracellular signal transduction while such details have not been observed with NASH. This difference may explain the tremendously higher incidence of HCC development in chronic hepatitis C patients than that in NASH patients. |