Fatty liver diseases, bile acids, and FXR

作者：Zhu, Yan; Liu, Hongxia; Zhang, Min; Guo, Grace L.^*

来源：Acta Pharmaceutica Sinica B, 2016, 6(5): 409-412.

DOI：10.1016/j.apsb.2016.07.008

• Nonalcoholic fatty liver disease
• Nonalcoholic steatohepatitis
• Liver metabolism
• Bile acids
• Farnesoid X receptor

The prevalence of nonalcoholic fatty liver disease (NAFLD) worldwide has increased at an alarming rate, which will likely result in enormous medical and economic burden. NAFLD presents as a spectrum of liver diseases ranging from simple steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and even to hepatocellular carcinoma (HCC). A comprehensive understanding of the mechanism(s) of NAFLD-to-NASH transition remains elusive with various genetic and environmental susceptibility factors possibly involved. An understanding of the mechanism may provide novel strategies in the prevention and treatment to NASH. Abnormal regulation of bile acid homeostasis emerges as an important mechanism to liver injury. The bile acid homeostasis is critically regulated by the farnesoid X receptor (FXR) that is activated by bile acids. FXR has been known to exert tissue-specific effects in regulating bile acid synthesis and transport. Current investigations demonstrate FXR also plays a principle role in regulating lipid metabolism and suppressing inflammation in the liver. Therefore, the future determination of the molecular mechanism by which FXR protects the liver from developing NAFLD may shed light to the prevention and treatment of NAFLD.

• 出版日期2016-9
• 单位中国人民解放军第三０二医院; 北京中医药大学