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
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/247114
- author
- Pereverzev, A ; Salehi, A ; Mikhna, M ; Renström, Erik LU ; Hescheler, J ; Weiergraber, M ; Smyth, N and Schneider, T
- organization
- publishing date
- 2005
- 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
- 2016-04-01 11:58:19
- date last changed
- 2022-01-26 20:55:06
@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}},
keywords = {{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}},
doi = {{10.1016/j.ejphar.2005.01.044}},
volume = {{511}},
year = {{2005}},
}