Improvement of Insulin Secretion in Diabetics by a Prostaglandin Synthesis Inhibitor

Abstract

Loss of first phase insulin secretion (the acute insulin response) which normally occurs 3–5 minutes after an intravenous glucose pulse is characteristic of patients with fasting hyperglycemia (1). This observation is of interest for several reasons. The acute insulin response (AIR) is probably lost relatively early in the pathogenesis of diabetes since it is absent when circulating glucose levels are only slightly elevated and at a time when basal insulin and second phase insulin secretion are probably normal. A second reason is that the loss of the AIR in hyperglycemic, non-insulin-dependent diabetics is only to glucose stimulation. Acute responses to intravenous isoproterenol and arginine, for instance, remain intact (2,3) despite absent responses to glucose. This suggests a defect related to an abnormality in glucose recognition by the beta cell rather than inadequacy of insulin synthesis or stores in the islet, i.e., the postulated “glucoreceptor” defect. A third reason this defect is of interest lies in the fact that absent first phase insulin secretion is restorable by alpha adrenergic blockade with phentolamine (4).