Abstract
Summary
Plasma glucose rose linearly with increasing amounts of glutamate up to a maximal dose of 0.2 mmoles/100 g body weight. The glutamate effect could not be explained by stoichiometric conversion of glutamate to glucose. Glutamate produced hyper-glycemia after 14-hour fast, at which time glucagon had no effect on glucose concentration. Adrenalectomy abolished the glutamate effect; ACTH suppression with dexametha-sone did not. Glutamate supplementation increased the plasma glucose response to pyruvate in excess of the additive effects of either substrate alone. It is suggested that glutamate produces hyperglycemia by stimulating new glucose production, and that this most likely results from increased glu-coneogenesis.
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