【正文】
anisms are illustrated in Figure 3. Metabolic Syndrome and HCC FIGURE 3. The pathogenesis of nonalcoholic fatty liver disease(NAFLD) is illustrated. IRS1 indicates insulin receptor substrate 1。 HCC, hepatocellular with permission from John Wiley amp。 PPAR, peroxisome proliferatoractivated receptor。 HCV, hepatitis C virus。 NASH,nonalcoholic steatohepatitis。 TNFa, tumor necrosis factor a。 95% CI, ), whereas for those who were obese, the relative risk was even higher at (95% CI,). Metabolic Syndrome and HCC ? Although earlier studies did not demonstrate a clear correlation between diabetes and HCC risk, more recent epidemiologic data suggest that diabetes likely is associated with a 2fold to 4fold increased risk of HCC. ? It is not known whether insulin resistance causes NASH. Patients with cirrhosis of all types may bee insulin resistant within the liver, because insulin is not cleared properly. Metabolic Syndrome and HCC ? However, it is believed that peripheral insulin resistance is ‘‘primary’’ and leads to hepatic steatosis, which then can contribute to both peripheral and hepatic insulin resistance. ? Steatosis, or fatty liver, also can be observed in patients with HCV infection, and those with both HCV and fatty liver changes have a greater risk of HCC than those with HCV alone. Thus, mechanisms of carcinogenesis may relate at least in part to the intermediate steps of fatty change in the liver and insulin resistance rather than the ‘‘final oute’’ of cirrhosis. Metabolic Syndrome and HCC ? Available data suggest that diabetes precedes