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In the course of chronic hepatitis C, various metabolic disorders have been observed with a higher frequency than in the general population. For example, the frequency of liver steatosis is 2.5-fold higher than in uninfected subjects, the majority of HCV-positive patients show insulin resistance, serum lipid levels are decreased in contrast to nonalcoholic fatty liver disease, obesity is detected in a higher proportion of HCVpositive patients than in the uninfected population, and epidemiological data confirm a relationship between chronic HCV infection and diabetes mellitus type 2. In another words, chronic C hepatitis presents with some elements of so-called metabolic syndrome and can be considered a metabolic liver disease possibly requiring adjuvant anti-steatotic treatment combined with antiviral therapy. It remains to be established whether the relationship between steatosis and HCV infection is causal or a direct pathogenic effect of the virus. Two possible mechanisms of fatty liver development are suggested in the group of HCV-positive patients: steatosis secondary to obesity ("metabolic steatosis" as a manifestation of metabolic syndrome) in genotype 1 and 4 infection and steatosis secondary to HCV infection ("viral steatosis") in genotype 3a infection. Metabolic steatosis seems to be multifactorial due to the interference of HCV with lipid secretion, degradation, and synthesis. The diabetogenic effect of HCV is probably a results of insulin resistance and chronic inflammatory reaction mediated by pro-inflammatory cytokines, especially TNF-α. As a consequence of insulin resistance, compensatory hyperinsulinism develops and glucose levels increase. In predisposed subjects these metabolic disturbances lead to fixed glucose intolerance and finally to diabetes mellitus. Metabolic abnormalities may promote various cardiovascular disorders. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) covers a wide spectrum of liver pathology - from steatosis alone, through the necroinflammatory disorder of nonalcoholic steatoheatohepatitis (NASH) to cirrhosis and liver cancer. NAFLD is recognized as one of the most frequent reason of liver test elevation. NAFLD/NASH is not a benign disease: progressive liver biopsy have shown histological progression of fibrosis in 32%, the estimated rate of cirrhosis development is 20% and a liver-related death is 12% over 10 years. No treatment has scientifically proved to ameliorate NAFLD or to avoid its progression and the therapeutic strategies are aimed at interfering with all pathogenetic factors of the disease. Insulin resistance is recently considering a key-player in NAFLD pathogenesis and the effort should be done to early detection of patients in risk of NAFLD development. The aim of this paper is to show the recent knowledge about insulin resistance and its clinical implications. [ABSTRACT FROM AUTHOR]