Author: Zhang Q. Berggren P.O. Larsson O. Hall K. Tally M.
Publisher: Elsevier
ISSN: 0006-291X
Source: Biochemical and Biophysical Research Communications, Vol.243, Iss.1, 1998-02, pp. : 117-121
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Abstract
We have investigated the effect of IGF-II on glucose-induced insulin release in the pancreatic beta-cell. Introduction of IGF-II during perifusion of the cells with 20 mM glucose abolished glucose-induced insulin release. Concomitant addition of IGF-II with 20 mM glucose caused a complete inhibition of insulin release. In addition, IGF-II inhibited Ca2+-induced insulin release from electropermeabilized pancreatic beta-cells. IGF-II had no effect on K+-or tolbutamide-induced insulin release. However, IGF-II could suppress K+-stimulated insulin release when cells were pretreated with the protein phosphatase inhibitor okadaic acid. The inhibitory effect of IGF-II on insulin release was not associated with significant changes in membrane potential, activity of the voltage-gated L-type Ca2+-channel or cytoplasmic free Ca2+ concentration. Pretreatment of the cells with pertussis toxin or the phorbol ester TPA abolished the inhibitory action of IGF-II on insulin release. Hence, the molecular mechanism whereby activation of the IGF-II/M6P receptor by IGF-II inhibits glucose-stimulated insulin exocytosis in the pancreatic beta-cell involves pertussis toxin-sensitive G proteins and is dependent on PKC activity. Copyright 1998 Academic Press.
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