Steatosis is a common feature of many liver diseases, namely non-alcoholic steatohepatitis (NASH) and hepatitis C virus (HCV) infection, but the pathogenic mechanisms differ. Insulin resistance (IR), a key feature of metabolic syndrome, is crucial for NASH development, associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to fibrosis. This may have potential implications for new drug therapy. In HCV-related disease, steatosis impacts both fibrosis progression and response to treatment. Steatosis in HCV-related disease relates to both viral factors (HCV genotype 3), and host factors (alcohol consumption, overweight, hyperlipidemia, diabetes). Among others, IR is a recognized factor. Hepatic steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its receptors. Thus, hepatic steatosis should not be considered a benign feature, but rather a silent killer.

Both hepatitis C infection and non-alcoholic fatty liver disease (NAFLD) are major causes of liver related morbidity and mortality. Hepatitis C virus (HCV) is a major cause of chronic liver disease with about 170 million people infected worldwide. The severity of disease varies widely from asymptomatic chronic infection to cirrhosis and hepatocellular carcinoma (HCC)

NAFLD represents a spectrum of liver diseases characterized mainly by macrovesicular steatosis that occurs in the absence of alcoholic consumption. The hepatic histology varies from isolated hepatic steatosis alone “first hit” to fatty liver accompanied by hepatocellular damage plus inflammation known as steatohepatitis “second hit” which is followed by the development of fibrosis.

Adipose tissue is now recognized as not simply a storage depot for excess energy, but rather an active endocrine organ that secretes a number of molecules termed, adipocytokines. A number of these adipocytokines have been linked to alterations in insulin sensitivity, including adiponectin, leptin,