title: Metabolic effects of bile acid sequestration: impact on cardiovascular risk factors.
abstract: OBJECTIVE
  This article discusses the impact of bile acid sequestrants (BAS) on cardiovascular risk factors (CVRFs), on the basis of recent (pre)clinical studies assessing the metabolic impact of modulation of enterohepatic bile acid signaling via the bile acid receptors farnesoid X receptor (FXR) and Takeda G-protein-coupled receptor 5 (TGR5).
  
  
  RESULTS
  BAS decrease low-density lipoprotein-cholesterol by stimulating de novo hepatic bile acid synthesis and lowering intestinal lipid absorption, and improve glucose homeostasis in type 2 diabetes mellitus, at least in part by increasing GLP-1 production, via intestinal TGR5- and FXR-dependent mechanisms. Intestinal and peripheral FXR and TGR5 modulation also affects peripheral tissues, which can contribute to the reduction of CVRFs.
  
  
  CONCLUSIONS
  Bile acids are regulators of metabolism acting in an integrated interorgan manner via FXR and TGR5. Modulation of the bile acid pool size and composition, and selective interference with their receptors could, therefore, be a therapeutic approach to decrease CVRFs. Even though clinical cardiovascular outcome studies using BAS are still lacking, the existing data point to BAS as an efficacious pharmacological approach to reduce CVRFs.
authors: aUniv Lille, UMR1011, EGID bInserm, UMR1011 cCHU Lille dInstitut Pasteur de Lille, U1011, Lille, France *Valeria Spinelli and Oscar Chávez-Talavera have contributed equally to the writing of this article.
authors: Valeria
authors: V
authors: Spinelli
authors: Oscar
authors: O
authors: Chávez-Talavera
authors: Anne
authors: A
authors: Tailleux
authors: Bart
authors: B
authors: Staels
mesh_terms: D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D050171:Dyslipidemias / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects; D018160:Receptors, Cytoplasmic and Nuclear / Q000187:drug effects / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000187:drug effects / Q000378:metabolism; D018570:Risk Assessment; D012307:Risk Factors; D064449:Sequestering Agents / Q000627:therapeutic use*; D015398:Signal Transduction / Q000187:drug effects; D016896:Treatment Outcome; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D001647:Bile Acids and Salts; D001786:Blood Glucose; D018160:Receptors, Cytoplasmic and Nuclear; D043562:Receptors, G-Protein-Coupled; D064449:Sequestering Agents; D000099150:Receptor, Farnesoid X-Activated; C473772:GPBAR1 protein, human