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Bile acids and nonalcoholic fatty liver disease: Molecular insights and therapeutic perspectives
Author(s) -
Arab Juan P.,
Karpen Saul J.,
Dawson Paul A.,
Arrese Marco,
Trauner Michael
Publication year - 2017
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.28709
Subject(s) - farnesoid x receptor , nonalcoholic fatty liver disease , bile acid , cirrhosis , hepatology , liver disease , medicine , ursodeoxycholic acid , g protein coupled bile acid receptor , disease , fatty liver , bioinformatics , gastroenterology , biology , nuclear receptor , biochemistry , transcription factor , gene
Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and an important risk factor for both hepatic and cardiometabolic mortality. The rapidly increasing prevalence of this disease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic approaches to prevent disease progression to advanced fibrosis or cirrhosis and cancer. In recent years, bile acids have emerged as relevant signaling molecules that act at both hepatic and extrahepatic tissues to regulate lipid and carbohydrate metabolic pathways as well as energy homeostasis. Activation or modulation of bile acid receptors, such as the farnesoid X receptor and TGR5, and transporters, such as the ileal apical sodium‐dependent bile acid transporter, appear to affect both insulin sensitivity and NAFLD/NASH pathogenesis at multiple levels, and these approaches hold promise as novel therapies. In the present review, we summarize current available data on the relationships of bile acids to NAFLD and the potential for therapeutically targeting bile‐acid‐related pathways to address this growing world‐wide disease. (H epatology 2017;65:350‐362)