Key result
Current murine models can recapitulate certain aspects of NAFLD and NASH, such as steatosis and mild inflammation, but no single model represents the full human disease spectrum.
Selecting an appropriate murine model to study NAFLD or NASH requires careful consideration of the specific disease pathology being investigated, as no single model perfectly mimics human disease progression in the context of obesity.
Clinicians should interpret murine NAFLD/NASH data cautiously; leaves open development of more representative models.
Associated with the obesity epidemic, non-alcoholic fatty liver disease (NAFLD) has become the leading liver disease in North America. Approximately 30 % of patients with NAFLD may develop non-alcoholic steatohepatitis (NASH) that can lead to cirrhosis and hepatocellular carcinoma (HCC). Frequently animal models are used to help identify underlying factors contributing to NAFLD including insulin resistance, dysregulated lipid metabolism and mitochondrial stress. However, studying the inflammatory, progressive nature of NASH in the context of obesity has proven to be a challenge in mice. Although the development of effective treatment strategies for NAFLD and NASH is gaining momentum, the field is hindered by a lack of a concise animal model that reflects the development of liver disease during obesity and the metabolic syndrome. Therefore, selecting an animal model to study NAFLD or NASH must be done carefully to ensure the optimal application. The most widely used animal models have been reviewed highlighting their advantages and disadvantages to studying NAFLD and NASH specifically in the context of obesity.
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Reid et al. (2015) conducted a review in Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Murine models (genetic and dietary) was evaluated. Current murine models can recapitulate certain aspects of NAFLD and NASH, such as steatosis and mild inflammation, but no single model represents the full human disease spectrum.
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