| Lipotoxicity impairs incretin signalling. | |
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MedLine Citation:
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PMID: 23188391 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic peptide are secreted by enteroendocrine cells and augment glucose-induced insulin secretion in response to food ingestion in a glucose-dependent manner. This mechanism forms the basis for incretin-based therapies in type 2 diabetes. However, the insulinotropic effect of incretins is diminished in type 2 diabetic patients, due in part to reduced expression of incretin receptors as a consequence of glucotoxicity. In this issue of Diabetologia, Kang et al (DOI: 10.1007/s00125-012-2776-x ) provide evidence that in addition to glucotoxicity, lipotoxicity also affects incretin receptor expression and signalling in insulin-secreting cells and isolated islets. In animal models of diabetes, the authors show that co-administration of a lipid-lowering drug with a dipeptidyl peptidase-4 inhibitor or a glucagon-like peptide-1 agonist improved glucose tolerance and beta cell mass. These novel findings provide convincing support for the notion that restoring normal circulating lipid levels in type 2 diabetes might help improve the efficacy of incretin-based therapies. |
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Authors:
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V Poitout |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-11-28 |
Journal Detail:
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Title: Diabetologia Volume: - ISSN: 1432-0428 ISO Abbreviation: Diabetologia Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-11-28 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0006777 Medline TA: Diabetologia Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Montreal Diabetes Research Center, CRCHUM, Technopôle Angus, 2901 Rachel Est, Montréal, QC, Canada, H1W 4A4, vincent.poitout@umontreal.ca. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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