Insulin secretion induced by glucose and by stimulation of β2-adrenoceptors in the rat. Different sensitivity to somatostatin

Abstract

The effects of somatostatin on insulin secretion stimulated by glucose or by the selective .beta.2-adrenoceptor agonist terbutaline were studied in vivo in the anesthetized rat. Infusion of low doses of glucose (5 mg/min) or terbutaline (2 .mu.g/min) caused slight stimulation of insulin secretion; infusion of higher doses of glucose (12.5 mg/min) or terbutaline (200 .mu.g/min) yielded higher rates of insulin release. In both instances plasma insulin concentrations were of comparable magnitudes immediately prior to somatostatin infusion. Somatostatin (0.1 .mu.g/min) inhibited the insulin response to glucose and terbutaline, both at the low and high secretory rates. The inhibitory effect of somatostatin was much more pronounced on insulin release during glucose infusion than during infusion of terbutaline. At the high rate of insulin secretion somatostatin depressed plasma insulin by 46% during glucose and by 22% during terbutaline infusion. The results at the low rate of insulin secretion were 66 and 48%, respectively. Both at high and low secretory rates somatostatin depressed plasma insulin levels more potently during glucose infusion than during terbutaline infusion (P < 0.001 and P < 0.05, respectively). The plasma insulin levels during inhibition by somatostatin following terbutaline stimulation stabilized after .apprx. 10 min of somatostatin infusion; following glucose stimulation the insulin levels continued to decline. Evidently, somatostatin inhibits insulin secretion via mechanisms that are more closely related to the insulin secretory pathway induced by glucose than to that induced by .beta.-adrenoceptor agonists.