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Disturbances in glucose-tolerance, insulin-release, and stress-induced hyperglycemia upon disruption of the Ca(V)2.3 (alpha 1E) subunit of voltage-gated Ca2+ channels

Record type: Article

Multiple types of voltage-activated Ca2+ channels (T, L, N, P, Q, R type) coordinate Ca2+-dependent processes in neurons and neuroendocrine cells. Expressional and functional data have suggested a role for Cav2.3 Ca2+ channels in endocrine processes. To verify its role in vivo, Cav2.3(-/-) mutant mice were generated, thus deficient in {alpha}1E/R-type Ca2+ channel. Intraperitoneal injection of D-glucose showed that glucose tolerance was markedly reduced, and insulin release into plasma was impaired in Cav2.3-deficient mice. In isolated islets of Langerhans from these animals, no glucose-induced insulin release was detected. Further, in stressed Cav2.3-deficient mice, the rate of glucose release into the blood was only 29% of that observed for wild-type animals. Thus, the deletion of Cav2.3 causes deficits not only in insulin release but also in stress-induced hyperglycemia. The complex phenotype of Cav2.3-deficient mice has dual components related to endocrine and neurological defects. The present findings provide direct evidence of a functional role for the Cav2.3 subunit in hormone secretion and glucose homeostasis.

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Citation

Pereverzev, A., Mikhna, M., Vajna, R., Gissel, C., Henry, M., Weiergraber, M., Hescheler, J., Smyth, N. and Schneider, T. (2002) Disturbances in glucose-tolerance, insulin-release, and stress-induced hyperglycemia upon disruption of the Ca(V)2.3 (alpha 1E) subunit of voltage-gated Ca2+ channels Molecular endocrinology, 16, (4), pp. 884-895.

More information

Published date: 1 April 2002

Identifiers

Local EPrints ID: 56119
URI: http://eprints.soton.ac.uk/id/eprint/56119
ISSN: 0888-8809
PURE UUID: 780f96da-0f65-4c53-a11e-f809f0bafabb

Catalogue record

Date deposited: 08 Aug 2008
Last modified: 17 Jul 2017 14:31

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Contributors

Author: A. Pereverzev
Author: M. Mikhna
Author: R. Vajna
Author: C. Gissel
Author: M. Henry
Author: M. Weiergraber
Author: J. Hescheler
Author: N. Smyth
Author: T. Schneider

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