Somatostatin-Induced Inhibition of Insulin Secretion from Isolated Islets of Rat Pancreas in Presence of Glucagon[*]

Abstract

In order to study the effect of somatostatin on the endocrine pancreas directly, islets isolated from rat pancreas by collagenase were incubated for 2 hrs 1) at 50 and 200 mg/100 ml glucose in the absence and presence of somatostatin (1, 10 and 100 ng/ml) and 2) at 200 mg/100 ml glucose together with glucagon (5 µg/ml), with or without somatostatin (100 ng/ml). Immunologically measurable insulin was determined in the incubation media at 0, 1 and 2 hrs.

Insulin release was not statistically affected by any concentration of somatostatin. On the other hand, somatostatin exerted a significant inhibitory action on glucagon-potentiated insulin secretion (mean ± SEM, µU/2 hrs/10 islets: glucose and glucagon: 1253 ± 92; glucose, glucagon and somatostatin: 786 ± 76). The insulin output in the presence of glucose, glucagon and somatostatin was also significantly smaller than in the presence of glucose alone (1104 ± 126) or of glucose and somatostatin (1061 ± 122).

The failure of somatostatin to affect glucose-stimulated release of insulin from isolated islets contrasts its inhibitory action on insulin secretion as observed in the isolated perfused pancreas and in vivo. This discrepancy might be ascribed to the isolation procedure using collagenase. However, somatostatin inhibited glucagon-potentiated insulin secretion in isolated islets which resulted in even lower insulin levels than obtained in the parallel experiments without glucagon. It is concluded that the hormone of the alpha cells, or the cyclic AMP system, might play a part in the mechanism of somatostatin-induced inhibition of insulin release from the beta-cell.

Key words

Somatostatin - Isolated Pancreatic Islets - Beta-cells - Insulin Secretion - Glucagon-Potentiated Insulin Secretion

1 Supported by Deutsche Forschungsgemeinschaft Bad Godesberg SFB 87, Ulm D 1

1 Supported by Deutsche Forschungsgemeinschaft Bad Godesberg SFB 87, Ulm D 1

2 Alexander von Humboldt-Fellow 1974/75, on leave from the Department of Endocrinology and Metabolism, Medical School, Cracow, Poland