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Interaction of Amino Acids and Cyclic AMP on the Release of Insulin and Glucagon by Newborn Rat Pancreas

Unité de Recherche de Diabetologie et d'Etudes Radio-Immunologiques des Hormones Proteiques U.55 (INSERM), Hôpital Saint-Antoine 75571 Paris-Cedex 12, France

Abstract

Splenic lobes from the pancreas of newborn rats (48–64 hr) were used for the in vitro investigation of cyclic AMP, glucose and amino acid interaction in hormonal secretion. The slight discrepancy found in glucagon release with radioimmunoassay and binding assay to specific receptors in liver does not affect the ratio of stimulated to control values. The insulin release due to theophylline, dibutyryl cyclic AMP (dbcAMP) or to arginine is glucose-dependent as in adult rats and provides an index for the validity of the preparations. Glucose alone is efficient in stimulating insulin release but does not affect glucagon secretion; however, simultaneous addition of 10 mM arginine, alanine, and lysine (A.A.), or of arginine alone resulted in a higher glucagon release at 1.6 mM than at 16.7 mM glucose. Theophylline (5 mM) and dbcAMP (2 mM) induced a 2-fold increase in glucagon release at low or high glucose concentrations.

Incubation of theophylline (10 mM) or dbcAMP (6 mM) and A.A. or arginine resulted in a considerable increase in glucagon release. Potentiation of the 3 A.A.-induced glucagon release by dbcAMP was about 1800% no matter what the glucose concentration; similar observations were made for insulin with a 700% potentiation of the 3 A.A. effect. Glucagon was released more effectively by dbcAMP than was insulin, whereas the reverse was observed with theophylline.

These findings suggest that knowledge of the cyclic AMP content is essential when assessing the influence of substrates on glucagon release. The combination of substrates with cyclic AMP clearly demonstrated that potentiation of glucagon release occurs mainly with amino acids, whereas for insulin release it is mainly glucose which potentiates release. (Endocrinology 96: 168, 1975)

Received July 11, 1974.

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