| Investigating the effects of physiological bile acids on GLP-1 secretion and glucose tolerance in normal and GLP-1R(-/-) mice. | |
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MedLine Citation:
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PMID: 21521075 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Abstract Physiological secretion of bile acids has previously been linked to the regulation of blood glucose. GLP-1 is an intestinal peptide hormone with important glucose-lowering actions, such as stimulation of insulin secretion and inhibition of glucagon secretion. In this investigation, we assessed the ability of several bile acid compounds to secrete GLP-1 in vitro in STC-1 cells. Bile acids stimulated GLP-1 secretion from 3.3- to 6.2-fold but some were associated with cytolytic effects. Glycocholic and taurocholic acids were selected for in vivo studies in normal and GLP-1R(-/-) mice. Oral glucose tolerance tests revealed that glycocholic acid did not affect glucose excursions. However, taurocholic acid reduced glucose excursions by 40% in normal mice and by 27% in GLP-1R(-/-) mice, and plasma GLP-1 concentrations were significantly elevated 30 min post-gavage. Additional studies used incretin receptor antagonists to probe involvement of GLP-1 and GIP in taurocholic acid-induced glucose lowering. The findings suggest that bile acids partially aid glucose regulation by physiologically enhancing nutrient-induced GLP-1 secretion. However, GLP-1 secretion appears to be only part of the glucose-lowering mechanism and our studies indicate that the other major incretin GIP is not involved. |
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Authors:
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Eamon P Rafferty; Alastair R Wylie; Katharine H Hand; Chris E Elliott; David J Grieve; Brian D Green |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-4-27 |
Journal Detail:
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Title: Biological chemistry Volume: - ISSN: 1437-4315 ISO Abbreviation: - Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-4-27 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9700112 Medline TA: Biol Chem Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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School of Biological Sciences, Queen's University Belfast, BT9 5AG, UK. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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