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The permissive effect of glucose, tolbutamide and high K + on arginine stimulation of insulin release in isolated mouse islets

The permissive effect of glucose, tolbutamide and high K + on arginine stimulation of insulin... 125 30 30 8 8 M. P. Hermans W. Schmeer J. C. Henquin Unité de Diabétologie et Nutrition University of Louvain, Faculty of Medicine Brussels Belgium I Physiologisches Institut, University of Saarland Homburg/Saar FRG Summary Mouse islets were used to study how glucose modulates arginine stimulation of insulin release. At 3 mmol/l glucose, arginine (20 mmol/l) decreased the resting membrane potential of B cells by about 10 mV, but did not evoke electrical activity. This depolarisation was accompanied by a slight but rapid acceleration of 86 Rb + efflux and 45 Ca 2+ influx. However, 45 Ca 2+ efflux and insulin release increased only weakly and belatedly. When the membrane was depolarised by threshold (7 mmol/l) or stimulatory (10–15 mmol/l) concentrations of glucose, arginine rapidly induced or augmented electrical activity, markedly accelerated 86 Rb + efflux, 45 Ca 2+ influx and efflux, and triggered a strong and fast increase in insulin release. When glucose-induced depolarisation of the B-cell membrane was prevented by diazoxide, arginine lost all effects but those produced at low glucose. However, the delayed increase in release still exhibited some glucose-dependency. In contrast, depolarisation by tolbut amide, at low glucose, largely mimicked the permissive effect of high glucose. Depolarisation by high K + also amplified arginine stimulation of insulin release, but did not accelerate it as did glucose or tolbutamide. Omission of extracellular Ca 2+ abolished the releasing effect of arginine under all conditions. The results thus show that the permissive action of glucose mainly results from its ability to depolarise the B-cell membrane. It enables the small depolarisation by arginine itself to activate Ca channels more rapidly and efficiently. Changes in the metabolic state of B cells may also contribute to this permissive action by increasing the efficacy of the initiating signal triggered by arginine. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetologia Springer Journals

The permissive effect of glucose, tolbutamide and high K + on arginine stimulation of insulin release in isolated mouse islets

Diabetologia , Volume 30 (8) – Aug 1, 1987

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References (39)

Publisher
Springer Journals
Copyright
Copyright © 1987 by Springer-Verlag
Subject
Medicine & Public Health; Human Physiology; Internal Medicine; Metabolic Diseases
ISSN
0012-186X
eISSN
1432-0428
DOI
10.1007/BF00277325
Publisher site
See Article on Publisher Site

Abstract

125 30 30 8 8 M. P. Hermans W. Schmeer J. C. Henquin Unité de Diabétologie et Nutrition University of Louvain, Faculty of Medicine Brussels Belgium I Physiologisches Institut, University of Saarland Homburg/Saar FRG Summary Mouse islets were used to study how glucose modulates arginine stimulation of insulin release. At 3 mmol/l glucose, arginine (20 mmol/l) decreased the resting membrane potential of B cells by about 10 mV, but did not evoke electrical activity. This depolarisation was accompanied by a slight but rapid acceleration of 86 Rb + efflux and 45 Ca 2+ influx. However, 45 Ca 2+ efflux and insulin release increased only weakly and belatedly. When the membrane was depolarised by threshold (7 mmol/l) or stimulatory (10–15 mmol/l) concentrations of glucose, arginine rapidly induced or augmented electrical activity, markedly accelerated 86 Rb + efflux, 45 Ca 2+ influx and efflux, and triggered a strong and fast increase in insulin release. When glucose-induced depolarisation of the B-cell membrane was prevented by diazoxide, arginine lost all effects but those produced at low glucose. However, the delayed increase in release still exhibited some glucose-dependency. In contrast, depolarisation by tolbut amide, at low glucose, largely mimicked the permissive effect of high glucose. Depolarisation by high K + also amplified arginine stimulation of insulin release, but did not accelerate it as did glucose or tolbutamide. Omission of extracellular Ca 2+ abolished the releasing effect of arginine under all conditions. The results thus show that the permissive action of glucose mainly results from its ability to depolarise the B-cell membrane. It enables the small depolarisation by arginine itself to activate Ca channels more rapidly and efficiently. Changes in the metabolic state of B cells may also contribute to this permissive action by increasing the efficacy of the initiating signal triggered by arginine.

Journal

DiabetologiaSpringer Journals

Published: Aug 1, 1987

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