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Erik Renström

Erik Renström

Vice-chancellor

Erik Renström

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

Author

  • A Pereverzev
  • A Salehi
  • M Mikhna
  • Erik Renström
  • J Hescheler
  • M Weiergraber
  • N Smyth
  • T Schneider

Summary, in English

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.

Department/s

  • Diabetes - Islet Patophysiology

Publishing year

2005

Language

English

Pages

65-72

Publication/Series

European Journal of Pharmacology

Volume

511

Issue

1

Document type

Journal article

Publisher

Elsevier

Topic

  • Pharmacology and Toxicology

Keywords

  • R-type Ca2+ channel
  • toxin-resistant current
  • inactivation
  • gene
  • cholinergic
  • islets of Langerhans
  • peptide hormone-release

Status

Published

Research group

  • Diabetes - Islet Patophysiology

ISBN/ISSN/Other

  • ISSN: 1879-0712