Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis,which occurs in the absence of alcohol abuse.NAFLD\ncan evolve into progressive liver injury and fibrosis in the formof nonalcoholic steatohepatitis (NASH). Several animal models have\nbeen developed to attempt to represent the morphological, biochemical, and clinical features of human NASH. The actual review\npresents a critical analysis of the most commonly used experimental models of NAFLD/NASH development. These models can\nbe classified into genetic, nutritional, and a combination of genetic and nutritional factors. The main genetic models are ob/ob\nand db/db mutant mice and Zucker rats. The principal nutritional models employ methionine- and choline-deficient, high-fat,\nhigh-cholesterol and high-cholate, cafeteria, and high-fructose diets. Currently, associations between high-fructose and various\ncompositions of high-fat diets have been widely studied. Previous studies have encountered significant difficulties in developing\nanimal models capable of reproducing human NASH. Some models produce consistent morphological findings, but the induction\nmethod differs significantly compared with the pathophysiology of human NASH. Other models precisely represent the clinical\nand etiological contexts of this disease but fail to provide accurate histopathological representations mainly in the progression from\nsteatosis to liver fibrosis
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