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J. Biol. Chem., Vol. 277, Issue 36, 32883-32891, September 6, 2002
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From the Glucose increases insulin secretion by raising
cytoplasmic Ca2+
([Ca2+]i) in
The Elevation of Glutamate Content and the Amplification of
Insulin Secretion in Glucose-stimulated Pancreatic Islets Are Not
Causally Related*
§,,,, and¶
Unité d'Endocrinologie et
Métabolisme, University of Louvain Faculty of Medicine, B-1200
Brussels, Belgium and the § Unité Propre de Recherche
9023, Centre National de la Recherche Scientifique,
F-34094 Montpellier, France
-cells
(triggering pathway) and augmenting the efficacy of Ca2+ on
exocytosis (amplifying pathway). It has been suggested that glutamate
formed from 
-ketoglutarate is a messenger of the amplifying pathway
(Maechler, P., and Wollheim, C. B. (1999) Nature 402, 685-689). This hypothesis was tested with mouse islets depolarized with 30 mM KCl (+ diazoxide) or with a saturating
concentration of sulfonylurea. Because
[Ca2+]i was elevated under these
conditions, insulin secretion was stimulated already in 0 mM glucose. The amplification of secretion produced
by glucose was accompanied by an increase in islet glutamate. However,
glutamine (0.5-2 mM) markedly augmented islet glutamate without affecting insulin secretion, whereas glucose augmented secretion without influencing glutamate levels when these were elevated
by glutamine. Allosteric activation of glutamate dehydrogenase by BCH
(2-amino 2-norbornane carboxylic acid) lowered islet glutamate but
increased insulin secretion. Similar insulin secretion thus occurred at
very different cellular glutamate levels. Glutamine did not affect
islet [Ca2+]i and
pHi, whereas glucose and BCH slightly raised
pHi and either slightly decreased (30 mM KCl) or increased (tolbutamide)
[Ca2+]i. The general dissociation
between changes in islet glutamate and insulin secretion refutes a role
of -cell glutamate in the amplification of insulin secretion
by glucose.
*
This work was supported by Grant 3.4552.98 from the Fonds de
la Recherche Scientifique Médicale (Brussels), by Grant ARC 00/05-260 from the General Direction of Scientific Research of the
French Community of Belgium, by the Interuniversity Poles of Attraction
Program P5/3/20 Federal Office for Scientific, Technical, and Cultural
Affairs from Belgium, and by the Centre National de la Recherche
Scientifique (Paris).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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