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rdf:type |
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lifeskim:mentions |
umls-concept:C0015127,
umls-concept:C0017687,
umls-concept:C0017725,
umls-concept:C0022131,
umls-concept:C0205263,
umls-concept:C0205349,
umls-concept:C0205409,
umls-concept:C0439799,
umls-concept:C0547070,
umls-concept:C0596235,
umls-concept:C0871261,
umls-concept:C1314792,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1855585,
umls-concept:C2911692
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pubmed:issue |
1
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pubmed:dateCreated |
2005-3-21
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pubmed:abstractText |
Glucagon release upon hypoglycemia is an important homeostatic mechanism utilized by vertebrates to restore blood glucose to normal. Glucagon secretion itself is triggered by Ca2+ influx through voltage-gated ion channels, and the gene inactivation of R-type Ca2+ channels, with Ca(v)2.3 as the ion conducting subunit, has been shown to disturb glucose homeostasis. To understand how glucagon release may be affected in Ca(v)2.3-deficient mice, carbachol, insulin and glucose induced glucagon response was investigated. While the rise of insulin and glucose induced by carbachol is normal, mutant mice show an impaired glucagon-response. Further, the effect of insulin injection on glucagon levels was altered by the loss of the Ca(v)2.3 subunit. Ca(v)2.3-deficient mice are characterized by an impaired glucose suppression of glucagon release. This was most obvious at the level of isolated islets suggesting that Ca(v)2.3 containing R-type voltage-gated Ca2+ channels are involved in the glucose-mediated signalling to glucagon release in mice.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0014-2999
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
21
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pubmed:volume |
511
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
65-72
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15777780-Animals,
pubmed-meshheading:15777780-Blood Glucose,
pubmed-meshheading:15777780-Body Weight,
pubmed-meshheading:15777780-Calcium Channels,
pubmed-meshheading:15777780-Carbachol,
pubmed-meshheading:15777780-Cation Transport Proteins,
pubmed-meshheading:15777780-Female,
pubmed-meshheading:15777780-Genotype,
pubmed-meshheading:15777780-Glucagon,
pubmed-meshheading:15777780-Glucose,
pubmed-meshheading:15777780-Insulin,
pubmed-meshheading:15777780-Islets of Langerhans,
pubmed-meshheading:15777780-Male,
pubmed-meshheading:15777780-Mice,
pubmed-meshheading:15777780-Mice, Inbred C57BL,
pubmed-meshheading:15777780-Mice, Knockout,
pubmed-meshheading:15777780-Phenotype,
pubmed-meshheading:15777780-Time Factors
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pubmed:year |
2005
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pubmed:articleTitle |
The ablation of the Ca(v)2.3/E-type voltage-gated Ca2+ channel causes a mild phenotype despite an altered glucose induced glucagon response in isolated islets of Langerhans.
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pubmed:affiliation |
Institute of Neurophysiology, University of Cologne, Robert-Koch-Str. 39, D-50931 Köln, Germany; Center of Molecular Medicine Cologne, University of Cologne, Robert-Koch-Str. 39, D-50931 Köln, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
In Vitro,
Research Support, Non-U.S. Gov't
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