Animal models of nonalcoholic fatty liver disease and steatohepatitis

Hepatic accumulation of Hedgehog-reactive progenitors increases with severity of fatty liver damage in mice

“…35 Similar mechanisms underlie the pathogenesis of NASH. 36 Fatty livers are particularly vulnerable to ethionine-induced hepatotoxicity, rapidly accumulating hepatic progenitors when exposed to this drug. 3,37 Ethionine was administered in drinking water for 1 week, 37 and water consumption in the two groups of mice was similar.…”

“…To investigate this, we employed two well-accepted mouse models of oxidative liver injury, chronic NASH and acute ethionine-induced hepatotoxicity. 36,47 In both, inhibited proliferation of mature hepatocytes and compensatory expansion of hepatic progenitors have been demonstrated. 3,31,37,48,49 We hypothesized that Hh signaling was likely to be involved in the latter process, because Hh ligands orchestrate the development of many tissues, as well as remodeling of damaged epithelia in various adult organs.…”

Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

“…Experimental models based on voluntary food intake have been developed to induce hepatic steatosis in laboratory animals [2][3][4][5][6][7][8]. The nutritional models using complete diets resemble the human condition in that they contain amounts of lipids or carbohydrates that exceed the energy needs of the body.…”

Leptin-mediated neovascularization is a prerequisite for progression of nonalcoholic steatohepatitis in rats

“…10 A downside of the CDAA model is that it does not induce first-hit features (obesity, insulin resistance, and hyperglycemia). 9 Zucker rats, which lack functional leptin receptor due to a miss-sense mutation, have these first-hit conditions. 11 In the present study, a choline-deficient, amino acid-defined diet was given to Zucker rats to observe the pathological sequences of NASH under first-hit conditions.…”

“…The different animal models of NASH have been extensively reviewed. 9 Among them, we employed a choline-deficient, amino acid-defined (CDAA) diet model. This model induces histological processes similar to those of human NASH-namely, hepatic steatosis, steatohepatitis, liver fibrosis, cirrhosis, and HCC development associated with elevation of several markers of reactive oxygen species, such as TBARSs and 8-OHdG.…”