title: Bile acid signaling through farnesoid X and TGR5 receptors in hepatobiliary and intestinal diseases.
abstract: BACKGROUND
  The well-known functions of bile acids (BAs) are the emulsification and absorption of lipophilic xenobiotics. However, the emerging evidences in the past decade showed that BAs act as signaling molecules that not only autoregulate their own metabolism and enterohepatic recirculation, but also as important regulators of integrative metabolism by activating nuclear and membrane-bound G protein-coupled receptors. The present review was to get insight into the role of maintenance of BA homeostasis and BA signaling pathways in development and management of hepatobiliary and intestinal diseases.
  
  
  METHODS
  Detailed and comprehensive search of PubMed and Scopus databases was carried out for original and review articles.
  
  
  RESULTS
  Disturbances in BA homeostasis contribute to the development of several hepatobiliary and intestinal disorders, such as non-alcoholic fatty liver disease, liver cirrhosis, cholesterol gallstone disease, intestinal diseases and both hepatocellular and colorectal carcinoma.
  
  
  CONCLUSIONS
  Further efforts made in order to advance the understanding of sophisticated BA signaling network may be promising in developing novel therapeutic strategies related not only to hepatobiliary and gastrointestinal but also systemic diseases.
authors: Department of Pharmacology, Toxicology and Clinical Pharmacology, Faculty of Medicine, University of Novi Sad, Hajduk Veljkova 3, 21000 Novi Sad, Serbia. bojan.s@uns.ac.rs.
authors: Bojan
authors: B
authors: Stanimirov
authors: Karmen
authors: K
authors: Stankov
authors: Momir
authors: M
authors: Mikov
mesh_terms: D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D001660:Biliary Tract Diseases / Q000378:metabolism* / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D007410:Intestinal Diseases / Q000378:metabolism* / Q000503:physiopathology; D008107:Liver Diseases / Q000378:metabolism* / Q000503:physiopathology; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D015398:Signal Transduction; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D001647:Bile Acids and Salts; D018160:Receptors, Cytoplasmic and Nuclear; D043562:Receptors, G-Protein-Coupled; D000099150:Receptor, Farnesoid X-Activated; C473772:GPBAR1 protein, human