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

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

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)65-72
JournalEuropean Journal of Pharmacology
Volume511
Issue number1
DOIs
Publication statusPublished - 2005

Subject classification (UKÄ)

  • Pharmacology and Toxicology

Keywords

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

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