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Bispebjerg Hospital - a part of Copenhagen University Hospital
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Evidence connecting old, new and neglected glucose-lowering drugs to bile acid-induced GLP-1 secretion: A review

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DOI

  1. Liraglutide decreases postprandial fibroblast growth factor 19 and glucagon-like peptide 2, and increases postprandial cholecystokinin in individuals with obesity

    Research output: Contribution to conferenceConference abstract for conferenceResearchpeer-review

  2. The glucose-lowering effect of the bile acid sequestrant sevelamer in patients with type 2 diabetes is not mediated by glucagon-like peptide 1

    Research output: Contribution to conferenceConference abstract for conferenceResearchpeer-review

  3. The Glucagon-Like Peptide-1 Analog, Liraglutide Is a Safe and Effective Treatment of Bile Acid Malabsorption: A Proof of Concept Study

    Research output: Contribution to conferenceConference abstract for conferenceResearchpeer-review

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Bile acids are amphipathic water-soluble steroid-based molecules best known for their important lipid-solubilizing role in the assimilation of fat. Recently, bile acids have emerged as metabolic integrators with glucose-lowering potential. Among a variety of gluco-metabolic effects, bile acids have been demonstrated to modulate the secretion of the gut-derived incretin hormone glucagon-like peptide-1 (GLP-1), possibly via the transmembrane receptor Takeda G-protein-coupled receptor 5 and the nuclear farnesoid X receptor, in intestinal L cells. The present article critically reviews current evidence connecting established glucose-lowering drugs to bile acid-induced GLP-1 secretion, and discusses whether bile acid-induced GLP-1 secretion may constitute a new basis for understanding how metformin, inhibitors of the apical sodium-dependent bile acids transporter, and bile acid sequestrants - old, new and neglected glucose-lowering drugs - improve glucose metabolism.

Original languageEnglish
JournalDiabetes, Obesity and Metabolism
Pages (from-to)1214-1222
Number of pages8
ISSN1462-8902
DOIs
Publication statusPublished - Sep 2017

    Research areas

  • Journal Article, Review

ID: 51454608