Non alcoholic fatty liver diseases (NAFLD) are represented by two main pathological conditions, hepatic steatosis (HS) and non alcoholic steatohepatitis (NASH), which are characterized by the accumulation of fat in the liver. The diagnosis of these two entities is achieved by histology and neither imaging nor biochemical markers are accurate enough to discriminate them. At the contrary of HS, NASH features hepatocyte necrosis, inflammation and fibrosis of variable intensity that could progress and ultimately evolve to cirrhosis. Therefore, it is important to distinguish between HS and NASH in order to treat the patients accordingly. In this study, the investigators aim to understand the molecular mechanisms that govern the transition from benign steatosis to complicated NASH. The investigators will analyze by "Q-RT-PCR" and "DNA microarray" technologies in the liver of obese patients, the expression of genes that are susceptible to be involved in the pathogenesis of NAFLD and identify the potential signaling pathways responsible for the progression of the disease.

Inclusion Criteria:

• Group T(n=30): patient without central adiposity, without insulin resistance, operated for cholecystectomy or a benign liver tumor
• Group A (n=30): patient with central adiposity, insulin resistance and hepatic steatosis (histology).
• Group B (n=30): patient with central adiposity, insulin resistance and steatohepatitis ± hepatic fibrosis (histology).

Exclusion Criteria:

• viral or autoimmune hepatitis
• hematochromatosis
• alcohol consumption (> 20 g/24h women, >30 g/24h men)
• type 1 diabetes
• inflammation or infection before procedure
• abnormal hemostasis or coagulation- pregnancy

Primary care clinic