Adrenergic receptors and the onset of streptozotocin-induced diabetes in mice

Abstract

Abstract Treatment with yohimbine, an α 2 -adrenergic blocker, prior to the injection of a subdiabetogenic dose of streptozotocin (STZ) produced hyperglycemia and hypoinsulinemia in mice 7 days later. Prazosin, an α 1 -adrenergic blocker, was ineffective. The capacity of phentolamine and phenoxybenzamine to potentiate the diabetogenic effect of STZ was intermediate between that of yohimbine and prazosin. Propranolol and hexamethonium inhibited the potentiating action of yohimbine. Yohimbine enhanced the potentiating effect of isoproterenol on the STZ-induced diabetes. Acute changes in plasma glucose and insulin levels induced by STZ were potentiated by yohimbine but not by prazosin. The insulin releasing ability of the pancreatic islets 7 days after STZ was all but lost in mice pretreated with yohimbine but not with prazosin. These results suggest that the β- and α 2 -, not α 1 -, adrenergic system which modulates insulin release from pancreatic islets influences the response to the diabetogenic action of STZ in mice.