الفهرس 
MITOCHONDRIAOnly 14 pages are availabe for public view
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Abstract
Hepatic steatosis is a common problem that can be caused by obesity, ethanol toxicity or intake of a wide variety of therapeutic drug e.g. antiarrhythmic drugs. Steatosis of any etiology can be associated with the development of necroinflammation and fibrosis so called steatohepatitis, According to the etiology, steatohepatitis is classified into alcoholic (ASH) and non-alcoholic steatohepatitis (NASH). There are several animal models of hepatic steatosis classified according to the mechanisms: firstly, increased hepatic input (i.e. synthesis or uptake) of fats as rats with naturally occurring mutation that increase hepatic Hpogenesis, or rats with environmentally induced hepatic lipogenesis e.g. high sucrose diet, high fat diet, arginine deficient diet, chronic ethanol ingestion. Secondly, decreased hepatic elimination (out put) of fats e.g. mice with naturally occurring mutations that inhibit fatty acid oxidation, or rat with environmental inhibition of hepatic fatty acid oxidation e.g. treatment with antiarrhythmic drugs (e.g. amiodarone).