Effect of hydrocortisone on terbutaline stimulated insulin release from isolated pancreatic islets

Subchronic treatment with hydrocortisone (HC; 125 mg/kg, ip) in the rat for seven days significantly increased plasma insulin levels without affecting plasma glucose concentrations or insulinogenic indices. The role of the beta-adrenergic activity of the pancreatic beta cells in HC-induced hyperinsulinemia was assessed by determining if HC treatment would potentiate beta-adrenergic agonist-stimulated insulin release from isolated rat islets. Terbutaline (TB; 10(-3)M) and isolated islets from fasted rats were used to test this hypothesis since TB significantly increased insulin release in 300 mg/dl glucose-containing medium (HGM) from the islets of fasted but not of fed rats. Pancreatic islets from overnight-fasted control and HC-pretreated rats were incubated in HGM or HGM containing either 10(-3)TB, 10(-6)M HC, or both TB and HC. It was found that glucose-stimulated and TB-induced insulin release from HC-pretreated rat islets were not different from those of control rat islets. HC (10(-6)M) added in vitro did not affect glucose-stimulated or TB-induced insulin release from the islets of either control or HC-treated rats. In summary, it was found that the insulinotropic effect of TB depends on medium glucose concentration and the nutritional state of animals. However, the results do not support the hypothesis that the hyperinsulinemia caused by subchronic treatment with HC involves enhancement of the beta-adrenergic activity of the pancreatic beta cells.