The imidazoline RX871024 stimulates insulin secretion in pancreatic β-cells from mice deficient in KAPT channel function

Alexander M. Efanov, Marianne Hoy, Robert Bränström, Sergei V. Zaitsev, Mark A. Magnuson, Suad Efendic, Jesper Gromada, Per Olof Berggren

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

Effects of the imidazoline compound RX871024 on cytosolic free Ca2+ concentration ([Ca2+]i) and insulin secretion in pancreatic β-cells from SUR1 deficient mice have been studied. In β-cells from wild-type mice RX871024 increased [Ca2+]i by blocking ATP-dependent K+-current (KATP) and inducing membrane depolarization. In β-cells lacking a component of the KATP-channel, SUR1 subunit, RX871024 failed to increase [Ca2+]i. However, insulin secretion in these cells was strongly stimulated by the imidazoline. Thus, a major component of the insulinotropic activity of RX871024 is stimulation of insulin exocytosis independently from changes in KATP-current and [Ca2+]i. This means that effects of RX871024 on insulin exocytosis are partly mediated by interaction with proteins distinct from those composing the KATP-channel.

Original languageEnglish (US)
Pages (from-to)918-922
Number of pages5
JournalBiochemical and biophysical research communications
Volume284
Issue number4
DOIs
StatePublished - Jan 1 2001

Keywords

  • ATP-dependent K-channel
  • Cytosolic free Ca concentration
  • Imidazoline
  • Insulin secretion

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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