| Activation of the AMP-activated protein kinase enhances glucose-stimulated insulin secretion in mouse β-cells. | |
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MedLine Citation:
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PMID: 21099309 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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The AMP-activated protein kinase (AMPK) is one of the key players in cellular energy regulation adapting cellular demands to nutritional and metabolic variations. Oral antidiabetic drugs like metformin and glitazones (thiazolidinediones) are known to stimulate this enzyme. Besides their established action on peripheral organs including liver and muscles, it has been claimed that these drugs may affect β-cell function. However, it is still a matter of debate whether pharmacological AMPK stimulation increases or decreases insulin secretion. To study this point and to reveal mechanisms underlying changes in insulin secretion we used the specific AMPK activator AICAR and investigated its effects on stimulus-secretion coupling. Membrane potential and currents were measured by the patch-clamp technique, [Ca (2+)]c, mitochondrial membrane potential, and NAD(P)H by fluorescence techniques and insulin secretion by a radioimmunoassay. AICAR enhanced glucose-stimulated insulin release, an effect that can be attributed to the augmentation of electrical activity and [Ca (2+)]c resulting from an AICAR-evoked inhibition of the KATP current. This latter effect was not due to a direct interaction of AICAR with the KATP channels but was dependent on cell metabolism. AICAR did not affect mitochondrial membrane potential or NAD(P)H autofluorescence. Metformin mimicked the action of AICAR on electrical activity, [Ca (2+) ]c, and KATP current. However, compared to AICAR the effects were less pronounced and not sufficient to stimulate insulin secretion. In conclusion, activation of AMPK augments nutrient-induced insulin secretion. Thus, targeting AMPK of β-cells may. |
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Authors:
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Martina Düfer; Katja Noack; Peter Krippeit-Drews; Gisela Drews |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Islets Volume: 2 ISSN: 1938-2022 ISO Abbreviation: Islets Publication Date: 2010 May-Jun |
Date Detail:
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Created Date: 2010-11-24 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101495366 Medline TA: Islets Country: United States |
Other Details:
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Languages: eng Pagination: 156-63 Citation Subset: IM |
Affiliation:
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Institute of Pharmacy, Department of Pharmacology, University of Tübingen, Tübingen, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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