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Nonalcoholic fatty liver disease (NAFLD) is a metabolic syndrome in which excess fat accumulates in the liver without history of alcoholic abuse. NAFLD is the most frequent cause of liver damage which is classified into steatosis, steatohepatitis, and may progress to liver cirrhosis and hepatocellular carcinoma.
Induction of hepatic transformation in mice manipulates by stimulating imbalance between lipid catabolism
and free fatty acid reabsorption resulting in accumulation of fat especially triglyceride in the liver with hepatic pathophysiology and histopathology as that in human. The animal models of NAFLD are divided by NAFLD-inducible methods into 2 patterns, namely genetic modified and dietary supplement models. The genetic modified models are mice which have been configured or knocked out lipid synthesis related gene(s) including transgenic SREBP-1c, ob/ob, db/db, KK-Ay, PTEN10 null, PPAR-a knockout mice. On the other hand, the dietary supplement models are inducible by several patterns of diet, i.e., methionine and choline deficient food, high fat diet, cholesterol and chocolate, or fructose. The progress or development of NAFLD in each mouse model depends on the method and period of induction. Hence, the progress of NAFLD mice employed should be accordingly considered to the research objectives to achieve a precise and accurate result, and effectiveness of the outcome.
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