title: The role of bile acids in reducing the metabolic complications of obesity after bariatric surgery: a systematic review.
abstract: BACKGROUND
  Bariatric surgery is currently the most efficacious treatment for obesity and its associated metabolic co-morbidities, such as diabetes. The metabolic improvements occur through both weight-dependent and weight-independent mechanisms. Bile acids (BAs) have emerged as key signalling molecules that have a central role in modulating many of the physiological effects seen after bariatric surgery. This systematic review assesses the evidence from both human and animal studies for the role of BAs in reducing the metabolic complications of obesity following bariatric surgery.
  
  
  METHODS
  We conducted a systematic search of Medline and Embase databases to identify all articles investigating the role of BAs in mediating the metabolic changes observed following bariatric surgery in both animal and human studies. Boolean logic was used with relevant search terms, including the following MeSH terms: 'bile acids and salts', 'bariatric surgery', 'metabolic surgery', 'gastrointestinal tract/surgery' and 'obesity/surgery'.
  
  
  RESULTS
  Following database searches (n=1197), inclusion from bibliography searches (n=2) and de-duplication (n=197), 1002 search results were returned. Of these, 132 articles were selected for full-text review, of which 38 articles were deemed relevant and included in the review. The findings support the effects of BAs on satiety, lipid and cholesterol metabolism, incretins and glucose homoeostasis, energy metabolism, gut microbiota and endoplasmic reticulum stress following bariatric surgery. Many of these metabolic effects are modulated through the BA receptors FXR and TGR5. We also explore a possible link between BAs and carcinogenesis following bariatric surgery.
  
  
  CONCLUSIONS
  Overall there is good evidence to support the role of BAs in the metabolic effects of bariatric surgery through the above mechanisms. BAs could serve as a novel therapeutic pharmacological target for the treatment of obesity and its associated co-morbidities.
authors.affiliation: Department of Surgery and Cancer, St Mary's Hospital, Imperial College London, London, UK.
authors.forename: N C
authors.initials: NC
authors.lastname: Penney
authors.affiliation: Department of Surgery and Cancer, St Mary's Hospital, Imperial College London, London, UK.
authors.forename: J
authors.initials: J
authors.lastname: Kinross
authors.affiliation: Department of Surgery and Cancer, St Mary's Hospital, Imperial College London, London, UK.
authors.forename: R C
authors.initials: RC
authors.lastname: Newton
authors.affiliation: Department of Surgery and Cancer, St Mary's Hospital, Imperial College London, London, UK.
authors.forename: S
authors.initials: S
authors.lastname: Purkayastha
mesh_terms: D050110:Bariatric Surgery; D001647:Bile Acids and Salts / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D004734:Energy Metabolism; D000069196:Gastrointestinal Microbiome; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D054795:Incretins / Q000378:metabolism; D050356:Lipid Metabolism; D008659:Metabolic Diseases / Q000209:etiology* / Q000517:prevention & control / Q000601:surgery; D009767:Obesity, Morbid / Q000150:complications* / Q000378:metabolism / Q000601:surgery; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D016896:Treatment Outcome; D015431:Weight Loss; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D001647:Bile Acids and Salts; D005947:Glucose; D054795:Incretins; D018160:Receptors, Cytoplasmic and Nuclear; D043562:Receptors, G-Protein-Coupled; D000099150:Receptor, Farnesoid X-Activated