LAUSR

Mouse models of non-alcoholic fatty liver disease (NAFLD) are required to both elucidate the pathogenesis of the disease and also to assess therapeutic interventions. The first criterion for a useful model is that it reproduces the histopathology of the disease. NAFLD is characterized by centrilobular and macrovesicular steatosis. In non-alcoholic steatohepatitis (NASH), the steatosis is accompanied by intralobular inflammation and hepatocellular ballooning. Mallory's hyaline (eosinophilic, amorphous structures in the cytoplasm) may be present. There may also be glycogenated hepatic nuclei, megamitochondria, iron deposition, and fibrosis. Fibrosis usually originates in the perisinusoidal region of zone 3. As disease progresses, bridging fibrosis and then cirrhosis develop. Since the stage of fibrosis is the most important predictor of liver morbidity and mortality in patients with NASH, it is crucial that this aspect of the histopathology is prominent in the mouse model. This article is protected by copyright. All rights reserved.