Lessons from Mouse Models of High-Fat Diet-Induced NAFLD

International Journal of Molecular Sciences

Akinobu Nakamura¹ 

[1] Division of Immunology and Metabolism, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan; E-Mail:

关键词: hyperglycemia;    insulin resistance;    insulin signaling;    non-alcoholic fatty liver disease;    non-alcoholic steatohepatitis;    liver tumorigenesis;   

DOI  :  10.3390/ijms141121240

来源: mdpi

【 摘 要 】

Nonalcoholic fatty liver disease (NAFLD) encompasses a clinicopathologic spectrum of diseases ranging from isolated hepatic steatosis to nonalcoholic steatohepatitis (NASH), the more aggressive form of fatty liver disease that may progress to cirrhosis and cirrhosis-related complications, including hepatocellular carcinoma. The prevalence of NAFLD, including NASH, is also increasing in parallel with the growing epidemics of obesity and diabetes. However, the causal relationships between obesity and/or diabetes and NASH or liver tumorigenesis have not yet been clearly elucidated. Animal models of NAFLD/NASH provide crucial information, not only for elucidating the pathogenesis of NAFLD/NASH, but also for examining therapeutic effects of various agents. A high-fat diet is widely used to produce hepatic steatosis and NASH in experimental animals. Several studies, including our own, have shown that long-term high-fat diet loading, which can induce obesity and insulin resistance, can also induce NASH and liver tumorigenesis in C57BL/6J mice. In this article, we discuss the pathophysiology of and treatment strategies for NAFLD and subsequent NAFLD-related complications such as NASH and liver tumorigenesis, mainly based on lessons learned from mouse models of high-fat diet-induced NAFLD/NASH.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland