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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

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
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
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 Cav2.3 as the ion conducting subunit, has been shown to disturb glucose homeostasis. To understand how glucagon release may be affected in Cav2.3-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 Cav2.3 subunit. Cav2.3-deficient mice are characterized by an impaired glucose suppression of glucagon release. This was most obvious at the level of isolated islets suggesting that Cav2.3 containing R-type voltage-gated Ca2+ channels are involved in the glucose-mediated signalling to glucagon release in mice.
Islets of Langerhans, peptide hormone-release, cholinergic, gene inactivation, toxin-resistant current, R-type Ca2+ channel
0014-2999
65-72
Pereverzev, Alexey
f0b066f9-a980-4c49-b6aa-ea149b0e0fb1
Salehi, Albert
bf870185-1faa-4c4e-8608-d797beb23d0d
Mikhna, Marina
aae54b0e-6fe9-4778-b6c4-71a47424faa9
Renstrom, Erik
2b127c78-6d3b-461d-b194-907d6622f81c
Hescheler, Jurgen
1770a631-b857-4250-9223-d1b165fe58be
Weiergraber, Marco
b112142e-de89-46be-8227-e09ccf3b6b73
Smyth, Neil
0eba2a40-3b43-4d40-bb64-621bd7e9d505
Schneider, Toni
d6160fe2-9019-4e50-8b5d-a3658b513387
Pereverzev, Alexey
f0b066f9-a980-4c49-b6aa-ea149b0e0fb1
Salehi, Albert
bf870185-1faa-4c4e-8608-d797beb23d0d
Mikhna, Marina
aae54b0e-6fe9-4778-b6c4-71a47424faa9
Renstrom, Erik
2b127c78-6d3b-461d-b194-907d6622f81c
Hescheler, Jurgen
1770a631-b857-4250-9223-d1b165fe58be
Weiergraber, Marco
b112142e-de89-46be-8227-e09ccf3b6b73
Smyth, Neil
0eba2a40-3b43-4d40-bb64-621bd7e9d505
Schneider, Toni
d6160fe2-9019-4e50-8b5d-a3658b513387

Pereverzev, Alexey, Salehi, Albert, Mikhna, Marina, Renstrom, Erik, Hescheler, Jurgen, Weiergraber, Marco, Smyth, Neil and Schneider, Toni (2005) 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. European Journal of Pharmacology, 511 (1), 65-72. (doi:10.1016/j.ejphar.2005.01.044).

Record type: Article

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 Cav2.3 as the ion conducting subunit, has been shown to disturb glucose homeostasis. To understand how glucagon release may be affected in Cav2.3-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 Cav2.3 subunit. Cav2.3-deficient mice are characterized by an impaired glucose suppression of glucagon release. This was most obvious at the level of isolated islets suggesting that Cav2.3 containing R-type voltage-gated Ca2+ channels are involved in the glucose-mediated signalling to glucagon release in mice.

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More information

Published date: March 2005
Keywords: Islets of Langerhans, peptide hormone-release, cholinergic, gene inactivation, toxin-resistant current, R-type Ca2+ channel

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Local EPrints ID: 55973
URI: https://eprints.soton.ac.uk/id/eprint/55973
ISSN: 0014-2999
PURE UUID: 492be65c-f2d7-44f6-b842-2174e373d54f

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Date deposited: 07 Aug 2008
Last modified: 13 Mar 2019 20:35

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