Adipokines and Pathogenesis of Non Alcoholic Fatty Liver Disease

Non alcoholic fatty liver disease is the hepatic manifestation of meta­bolic syndrome that may progress from simple steatosis to nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. Expansion of omental adipose is accompanied by alteration in profiles of adi­pocytokines that contribute to NAFLD through enhanced steatogenesis in the liver and its inflammation. Gene transcription studies demon­strated a prominent adipose-specific deregulation of the inflammation and immune system related genes in NASH. Serum levels of soluble adipokines and cytokines can reliably predict NASH in the cohort of morbidly obese patients. Histologic fibrosis in patients with NASH could be predicted by TNF-α level. There is also strong connection between the HCV genotype 3, steatosis and increases in IL-8 serum levels. HCV genotype specific differences in soluble cytokine concentrations may help to elucidate pathogenesis of HCV hepatitis and potential triggers for HCV-related steatosis. These results should be of interest to the researchers of the clinical and fundamental aspects of human meta­bolism, obesity, diabetes, and hepatitis C.