الفهرس 
Non-alcoholic Fatty Liver DiseaseOnly 14 pages are availabe for public view
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is recognized as a common clinicopathological condition characterized by significant accumulation of lipid in the hepatocytes of the liver parenchyma leading to continuous abnormalities in liver enzyme. The increased prevalence of NAFLD has been associated with the epidemic of obesity. Although the histologic picture is similar to that of alcohol-induced liver injury, yet NAFLD occurs without significant alcohol abuse. Evidently, NAFLD includes a wide range of hepatic damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis, and cirrhosis. The outcome of NAFLD is now found to be a cause of end-stage liver disease and is accompanied by increased incidences of hepatocellular carcinoma (HCC), liver transplantation, and death.The development of NAFLD arises from the abnormal accumulation of triacylglycerol (TAG) in the liver as a result of an imbalance between TAG acquisition and removal. However, the factors which initiate NAFLD pathogenesis and which promote simple steatosis to NASH have not yet been fully understood. Conceivably, the classic “Two-hit” hypothesis for the pathogenesis of NAFLD has been introduced and modified by Day. The “first hit” which is closely related to obesity and to insulin resistance, increases the sensitivity of liver to a combination of both environmental and genetic “second hits”, which leads to NASH and fibrosis.