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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

Pereverzev, A; Salehi, A; Mikhna, M; Renström, Erik LU ; Hescheler, J; Weiergraber, M; Smyth, N and Schneider, T (2005) In European Journal of Pharmacology 511(1). p.65-72
Abstract
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.... (More)
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-deficientmice 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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
R-type Ca2+ channel, toxin-resistant current, inactivation, gene, cholinergic, islets of Langerhans, peptide hormone-release
in
European Journal of Pharmacology
volume
511
issue
1
pages
65 - 72
publisher
Elsevier
external identifiers
  • pmid:15777780
  • wos:000228028900008
  • scopus:15044358939
ISSN
1879-0712
DOI
10.1016/j.ejphar.2005.01.044
language
English
LU publication?
yes
id
cb296b35-b755-4e1e-a23e-440c99d4af8b (old id 247114)
date added to LUP
2007-10-05 12:09:32
date last changed
2017-03-26 03:32:32
@article{cb296b35-b755-4e1e-a23e-440c99d4af8b,
  abstract     = {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-deficientmice 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.},
  author       = {Pereverzev, A and Salehi, A and Mikhna, M and Renström, Erik and Hescheler, J and Weiergraber, M and Smyth, N and Schneider, T},
  issn         = {1879-0712},
  keyword      = {R-type Ca2+ channel,toxin-resistant current,inactivation,gene,cholinergic,islets of Langerhans,peptide hormone-release},
  language     = {eng},
  number       = {1},
  pages        = {65--72},
  publisher    = {Elsevier},
  series       = {European Journal of Pharmacology},
  title        = {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},
  url          = {http://dx.doi.org/10.1016/j.ejphar.2005.01.044},
  volume       = {511},
  year         = {2005},
}