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Somatostatin Modulation of Pancreatic Glucagon, Insulin, Glucose and Free Fatty Acids Following Beta-Adrenergic Stimulation

Department of Internal Medicine, Endocrinology and Metabolism, and Department of Nutrition and Metabolism, Center of Internal Medicine and Paediatrics, University of Ulm, 7900 Ulm, Federal Republic of Germany

This study was undertaken to determine the effect of somatostatin on acute, orciprenaline mediated, β-adrenergic stimulation of free fatty acids, blood glucose, insulin, and glucagon in healthy subjects. After orciprenaline and somatostatin insulin and glucagon decreased, whereas blood glucose and free fatty acids increased, probably in part as a result of the lesser inhibition of glucagon (50%) than of insulin (83%). From these observations it is tentatively concluded that the inhibitory effects of somatostatin on insulin and glucagon release in man are a consequence of β-adrenergic receptor involvement. These effects are possibly mediated through increased destruction of CAMP, blocking of CAMP dependent secretion or impairment of calcium uptake.

^* Present address: Servicio de Endocrinologia, Hospital Clinico, University of Granada/Spain.

Supported by a grant from the Deutsche Forschungsgemeinschaft (SFB 87/Endokrinologie).

Received September 28, 1976.