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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
113
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pubmed:dateCreated |
2010-3-17
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pubmed:abstractText |
Parasympathetic stimulation of pancreatic islets augments glucose-stimulated insulin secretion by inducing inositol trisphosphate receptor (IP(3)R)-mediated calcium ion (Ca2+) release. Ankyrin-B binds to the IP(3)R and is enriched in pancreatic beta cells. We found that ankyrin-B-deficient islets displayed impaired potentiation of insulin secretion by the muscarinic agonist carbachol, blunted carbachol-mediated intracellular Ca2+ release, and reduced the abundance of IP3R. Ankyrin-B-haploinsufficient mice exhibited hyperglycemia after oral ingestion but not after intraperitoneal injection of glucose, consistent with impaired parasympathetic potentiation of glucose-stimulated insulin secretion. The R1788W mutation of ankyrin-B impaired its function in pancreatic islets and is associated with type 2 diabetes in Caucasians and Hispanics. Thus, defective glycemic regulation through loss of ankyrin-B-dependent stabilization of IP3R is a potential risk factor for type 2 diabetes.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ank2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ankyrins,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Carbachol,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering
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pubmed:status |
MEDLINE
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pubmed:issn |
1937-9145
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pubmed:author |
pubmed-author:BennettVannV,
pubmed-author:BerggrenPer-OlofPO,
pubmed-author:BerglundJelenaJ,
pubmed-author:DavisJonathanJ,
pubmed-author:HealyJane AJA,
pubmed-author:HoffmanJanisJ,
pubmed-author:HohmeierHans EHE,
pubmed-author:KohlerMartinM,
pubmed-author:LiLuo-ShengLS,
pubmed-author:NewgardChristopher BCB,
pubmed-author:NilssonKent RKR
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pubmed:issnType |
Electronic
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
ra19
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:20234002-Animals,
pubmed-meshheading:20234002-Ankyrins,
pubmed-meshheading:20234002-Calcium,
pubmed-meshheading:20234002-Carbachol,
pubmed-meshheading:20234002-Diabetes Mellitus, Type 2,
pubmed-meshheading:20234002-Glucose,
pubmed-meshheading:20234002-Immunoblotting,
pubmed-meshheading:20234002-Inositol 1,4,5-Trisphosphate Receptors,
pubmed-meshheading:20234002-Insulin,
pubmed-meshheading:20234002-Insulin-Secreting Cells,
pubmed-meshheading:20234002-Mice,
pubmed-meshheading:20234002-Microscopy, Fluorescence,
pubmed-meshheading:20234002-Mutation, Missense,
pubmed-meshheading:20234002-Parasympathetic Nervous System,
pubmed-meshheading:20234002-Polymorphism, Single Nucleotide,
pubmed-meshheading:20234002-RNA, Small Interfering,
pubmed-meshheading:20234002-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20234002-Risk Factors
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pubmed:year |
2010
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pubmed:articleTitle |
Cholinergic augmentation of insulin release requires ankyrin-B.
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pubmed:affiliation |
1Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA.
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pubmed:publicationType |
Journal Article
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