The imidazoline RX871024 stimulates insulin secretion in pancreatic beta-cells from mice deficient in K(ATP) channel function.

Efanov AM, Høy M, Bränström R, Zaitsev SV, Magnuson MA, Efendic S, Gromada J, Berggren PO
Biochem Biophys Res Commun. 2001 284 (4): 918-22

PMID: 11409880 · DOI:10.1006/bbrc.2001.5068

Effects of the imidazoline compound RX871024 on cytosolic free Ca(2+) concentration ([Ca(2+)]i) and insulin secretion in pancreatic beta-cells from SUR1 deficient mice have been studied. In beta-cells from wild-type mice RX871024 increased [Ca(2+)]i by blocking ATP-dependent K(+)-current (K(ATP)) and inducing membrane depolarization. In beta-cells lacking a component of the K(ATP)-channel, SUR1 subunit, RX871024 failed to increase [Ca(2+)]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 K(ATP)-current and [Ca(2+)]i. This means that effects of RX871024 on insulin exocytosis are partly mediated by interaction with proteins distinct from those composing the K(ATP)-channel.

Copyright 2001 Academic Press.

MeSH Terms (22)

Animals Calcium Cells, Cultured Exocytosis Female Imidazoles Indoles Insulin Insulin Secretion In Vitro Techniques Islets of Langerhans Kinetics Membrane Potentials Mice Mice, Knockout Oocytes Potassium Channel Blockers Potassium Channels Potassium Channels, Inwardly Rectifying Promoter Regions, Genetic Reference Values Xenopus laevis

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