الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is considered as the most prevalent form of chronic liver diseases globally, which is characterized by extra fats build up in liver cells (˃ 5%) in the form of triglycerides that is not related to excessive alcohol consumption (1). Triglyceride (TG) accumulation in the hepatocytes is a pivotal hallmark in NAFLD pathogenesis that results from an imbalance between lipid removal (ie, β-oxidation of fatty acid within mitochondria as well as exportation as very low-density lipoprotein [VLDL] ) and acquisition (ie, uptake of fatty acids and de novo lipogenesis [DNL] ) (2). Today, NAFLD is considered to be the hepatic component of metabolic syndrome (3). Non-alcoholic fatty liver disease has become a serious health concern as a result of its increasing prevalence, difficulties in diagnosis, complex pathophysiology, and lack of approved therapies (4). NAFLD is actually a wide spectrum of diseases ranging from simple hepatic steatosis, where there is an accumulation of excessive fats in the liver cells to non alcoholic steatohepatitis (NASH), where the accumulated fat is combined with inflammation and cell damage, which then in the presence of additional factors can lead to fibrosis and finally cirrhosis and cell death may eventually occur.