Document Detail


Beneficial metabolic effects caused by persistent activation of beta-cell M3 muscarinic acetylcholine receptors in transgenic mice.
MedLine Citation:
PMID:  20843999     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies have shown that β-cell M(3) muscarinic acetylcholine receptors (M3Rs) play a key role in maintaining blood glucose homeostasis by enhancing glucose-dependent insulin release. In this study, we tested the hypothesis that long-term, persistent activation of β-cell M3Rs can improve glucose tolerance and ameliorate the metabolic deficits associated with the consumption of a high-fat diet. To achieve the selective and persistent activation of β-cell M3Rs in vivo, we generated transgenic mice that expressed the Q490L mutant M3R in their pancreatic β-cells (β-M3-Q490L Tg mice). The Q490L point mutation is known to render the M3R constitutively active. The metabolic phenotypes of the transgenic mice were examined in several in vitro and in vivo metabolic tests. In the presence of 15 mm glucose and the absence of M3R ligands, isolated perifused islets prepared from β-M3-Q490L Tg mice released considerably more insulin than wild-type control islets. This effect could be completely blocked by incubation of the transgenic islets with atropine (10 μm), an inverse muscarinic agonist, indicating that the Q490L mutant M3R exhibited ligand-independent signaling (constitutive activity) in mouse β-cells. In vivo studies showed that β-M3-Q490L Tg mice displayed greatly improved glucose tolerance and increased serum insulin levels as well as resistance to diet-induced glucose intolerance and hyperglycemia. These results suggest that chronic activation of β-cell M3Rs may represent a useful approach to boost insulin output in the long-term treatment of type 2 diabetes.
Authors:
Dinesh Gautam; Inigo Ruiz de Azua; Jian Hua Li; Jean-Marc Guettier; Thomas Heard; Yinghong Cui; Huiyan Lu; William Jou; Oksana Gavrilova; Walter S Zawalich; Jürgen Wess
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't     Date:  2010-09-15
Journal Detail:
Title:  Endocrinology     Volume:  151     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-21     Completed Date:  2010-11-04     Revised Date:  2013-02-27    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5185-94     Citation Subset:  AIM; IM    
Affiliation:
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 8 Center Drive MSC 0810, Bethesda, MD 20892-0810, USA.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Atropine / pharmacology
Blood Glucose / drug effects,  metabolism*
Genotype
Homeostasis / drug effects
Insulin / blood,  secretion
Insulin-Secreting Cells / drug effects,  metabolism*,  secretion
Mice
Mice, Transgenic
Muscarinic Antagonists / pharmacology
Phenotype
Receptor, Muscarinic M3 / genetics,  metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 0/Muscarinic Antagonists; 0/Receptor, Muscarinic M3; 51-55-8/Atropine
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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