2017, Number 1
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ABSTRACTNonalcoholic liver disease (NAFLD) is a major emerging health burden that is a common cause of illness and death worldwide. NAFLD can progress into nonalcoholic steatohepatitis (NASH) which is a severe form of liver disease characterized by inflammation and fibrosis. Further progression leads to cirrhosis, which predisposes patients to hepatocellular carcinoma or liver failure. The mechanism of the progression from simple steatosis to NASH is unclear. However, there are theories and hypothesis which support the link between disruption of the bile acids homeostasis and the progression of this disorder. Previous studies have been demonstrated that alterations of these pathways can lead to dysregulation of energy balance and an increase of liver inflammation and fibrosis. In this review, we summarized the current knowledge of the interaction between BA and the process related to the development of NAFLD, besides, the potential targets for novel therapies.
Bechmann LP, Kocabayoglu P, Sowa JP, Sydor S, Best J, Schlattjan M, Beilfuss A, et al. Free fatty acids repress small heterodimer partner (SHP) activation and adiponectin counteracts bile acid-induced liver injury in superobese patients with nonalcoholic steatohepatitis. Hepatology 2013; 4: 1394-406.