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

Abstract:

: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.

authors

Efanov AM,Høy M,Bränström R,Zaitsev SV,Magnuson MA,Efendic S,Gromada J,Berggren PO

doi

10.1006/bbrc.2001.5068

subject

Has Abstract

pub_date

2001-06-22 00:00:00

pages

918-22

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(01)95068-5

journal_volume

284

pub_type

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