Abstract
The insulin-releasing action of the amino acid arginine in man is inhibited by hypoglycemia. Furthermore, arginine potentiates glucose-induced insulin release, probably by amplifying the insulinogenic signal evoked by glucose in the beta-cell. The beta-adrenergic blocking agent propranolol, in doses known to suppress glucose-induced insulin release, did not alter insulin response to arginine infusion. Arginine markedly augments insulin release secondary to glucose whereas, under the same experimental conditions, it has no effect on insulin release secondary to glucagon. Finally, pretreatment with aminophylline potentiated the insulinogenic potency of the amino acid. We have previously postulated that glucose elicits insulin release by acting directly on a specific cell membrane receptor. The signal thus evoked is probably mediated through the adenyl cyclase-cyclic AMP system. In the light of this hypothesis and the above results we suggest that arginine acts on the beta-cell by amplifying the transmission...
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More From: The Journal of clinical endocrinology and metabolism
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