Glutamate stimulates insulin secretion and improves glucose
tolerance in rats.
Bertrand, G., R. Puech, M. M. Loubatieres-Mariani, and J. Bockaert.
CNRS UPR 9023, CCIPE, rue de la Cardonille, 34094 Montpellier Cedex
5 and Facult[acute]e de M[acute]edecine Laboratoire de Pharmacologie,
Institut de Biologie, Boulevard Henri IV, 34060 Montpellier Cedex 1,
France
APStracts 2:0093E, 1995.
We have previously shown in vitro that glutamate stimulates insulin
release via an AMPA receptor. Here we address a more physiological
question concerning the in vivo effect of glutamate, administered
intravenously or orally, on insulinemia and glycemia in fed and
fasted rats. In anaesthetized fed rats, the intravenous
administration of glutamate (9 and 30 mg/kg) transiently increased
insulinemia in a dose-dependent manner. The insulin secretory effect
of glutamate (9 mg/kg) was blocked by an antagonist of AMPA
receptors. In anaesthetized fasted rats, glutamate (9 mg/kg) was
ineffective, but during an intravenous glucose tolerance test (0.5
g/kg) glutamate markedly potentiated insulin release and increased
the glucose disappearance rate. In conscious rats, the intragastric
administration of glutamate (200 mg/kg) elicited a transient insulin
response in fed animals; had no effect in fasted animals but during
an oral glucose tolerance test (1 g/kg) enhanced insulin secretion
and reduced the hyperglycemia. Glutamate was effective at plasma
concentrations ranging 200-300 M. In conclusion, glutamate,
administered not only intravenously but also orally, stimulates
insulin secretion in vivo via an excitatory amino acid receptor and
improves glucose tolerance.
Received 23 February 1995; accepted in final form 21 April 1995.
APS Manuscript Number E75-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.