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Tytuł:
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Muscarinic Agonist Ameliorates Insulin Secretion in Wfs1-Deficient Mice.
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Autorzy:
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Toots M; Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia; Laboratory Animal Centre, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia. Electronic address: .
Reimets R; Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia; Laboratory Animal Centre, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Plaas M; Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia; Laboratory Animal Centre, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Vasar E; Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia; Centre of Excellence for Genomics and Translational Medicine, University of Tartu, Tartu, Estonia.
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Źródło:
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Canadian journal of diabetes [Can J Diabetes] 2019 Mar; Vol. 43 (2), pp. 115-120. Date of Electronic Publication: 2018 Jun 23.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Toronto : Canadian Diabetes Association, 2002-
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MeSH Terms:
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Carbachol/*pharmacology
Insulin Secretion/*drug effects
Membrane Proteins/*deficiency
Muscarinic Agonists/*pharmacology
Animals ; Blood Glucose ; Enzyme-Linked Immunosorbent Assay ; Glucose/pharmacology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout
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Contributed Indexing:
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Keywords: Wolframin1 (Wfs1); diabetes; diabète; hyperglycemia; hyperglycémie; insulin secretion; muscarinic receptor M3; récepteur muscarinique de sous-type M3 (récepteur M3); sécrétion d'insuline; wolframine 1 (WFS1)
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Substance Nomenclature:
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0 (Blood Glucose)
0 (Membrane Proteins)
0 (Muscarinic Agonists)
0 (wolframin protein)
8Y164V895Y (Carbachol)
IY9XDZ35W2 (Glucose)
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Entry Date(s):
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Date Created: 20180930 Date Completed: 20190730 Latest Revision: 20190730
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Update Code:
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20240105
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DOI:
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10.1016/j.jcjd.2018.06.007
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PMID:
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30266217
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Objectives: Similar to patients with Wolfram syndrome and to heterozygous Wolframin1 (Wfs1) mutation carriers, Wfs1-deficient mice exhibit impaired glucose tolerance and lower plasma insulin levels. Muscarinic receptor 3 agonists have previously been shown to potentiate glucose-stimulated insulin secretion. Therefore, the aim of this study was to investigate insulin-secretion dynamics in Wfs1-deficient mice and evaluate carbachol, muscarinic agonist and the ability to ameliorate the insulin secretion deficits caused by the Wfs1 mutation.
Methods: Wild-type Wfs1 heterozygous and Wfs1 mutant mice were used. Blood glucose was measured after glucose and carbachol administration. Insulin secretion was measured from serum using ELISA.
Results: Glucose administration causes hyperglycemia in Wfs1-deficient mice due to decreased insulin secretion. This deficit is abolished by administration of the muscarinic agonist carbachol.
Conclusions: Activation of the muscarinic pathway to potentiate insulin secretion may present a target to manage diabetes resulting from Wfs1 deficiency.
(Copyright © 2018 Diabetes Canada. Published by Elsevier Inc. All rights reserved.)
