The intraperitoneal administration of tranylcypromine, a nonhydrazine monoamine oxidase inhibitor, to mice resulted in a rapid and marked stimulation of insulin secretion, which was followed at 60 to 90 min. by profound hypoglycemia. The conversion of lactate to blood glucose was markedly depressed by the drug. Other monoamine oxidase inhibitors tested had no effect on insulin secretion or blood glucose. The tranylcypromine stimulated insulin secretion was not affected by prior administration of reserpine but was inhibited by prior administration of MJ 1999, a β-adrenergic receptor blocker. Tranylcypromine stimulated insulin secretion was augmented by prior administration of phentolamine, an α-adrenergic receptor blocker. Prostaglandin E1 administration stimulated insulin secretion and this effect was also inhibited by MJ 1999. Tranylcypromine stimulation of insulin secretion from the pancreas was also obtained in vitro. The role of α and β-adrenergic receptors in the control of insulin secretion in the pancreatic islets is discussed.