title: Bile acids and nonalcoholic fatty liver disease: Molecular insights and therapeutic perspectives.
abstract: 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. (Hepatology 2017;65:350-362).
authors.affiliation: Department of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
authors.forename: Juan P
authors.initials: JP
authors.lastname: Arab
authors.affiliation: Division of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
authors.forename: Saul J
authors.initials: SJ
authors.lastname: Karpen
authors.affiliation: Division of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
authors.forename: Paul A
authors.initials: PA
authors.lastname: Dawson
authors.affiliation: Department of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
authors.forename: Marco
authors.initials: M
authors.lastname: Arrese
authors.affiliation: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
authors.forename: Michael
authors.initials: M
authors.lastname: Trauner
mesh_terms: D001647:Bile Acids and Salts / Q000502:physiology*; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology; D050356:Lipid Metabolism; D008099:Liver; D064307:Microbiota; D065626:Non-alcoholic Fatty Liver Disease / Q000188:drug therapy* / Q000209:etiology* / Q000235:genetics; D018160:Receptors, Cytoplasmic and Nuclear / Q000819:agonists / Q000037:antagonists & inhibitors; D043562:Receptors, G-Protein-Coupled; D015398:Signal Transduction; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D001647:Bile Acids and Salts; D005947:Glucose; D018160:Receptors, Cytoplasmic and Nuclear; D043562:Receptors, G-Protein-Coupled; D000099150:Receptor, Farnesoid X-Activated; C473772:GPBAR1 protein, human