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


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), 884-895.

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Description/Abstract

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.

Item Type: Article
ISSNs: 0888-8809 (print)
Related URLs:
Subjects: Q Science > Q Science (General)
R Medicine > R Medicine (General)
Divisions: University Structure - Pre August 2011 > School of Biological Sciences
ePrint ID: 56119
Date Deposited: 08 Aug 2008
Last Modified: 27 Mar 2014 18:38
URI: http://eprints.soton.ac.uk/id/eprint/56119

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