W\e have reported previously that the oral or intravenous administration of the amino acid l-leucine to healthy subjects results in increases in plasma insulin and decreases in blood glucose and plasma free fatty acids (2, 3). After the administration of leucine to healthy subjects pretreated with either chlorpropamide or tolbutamide (2, 3), and also to some patients with functioning islet cell tumors of the pancreas (4), increments in plasma leucine caused increases in plasma insulin and decreases in blood glucose that were significantly greater than those observed in healthy subjects not pretreated with sulfonylurea drugs. We have also shown that increased release of insulin from the pancreatic beta cells is the mechanism by which leucine increases peripheral levels of insulin (5). We suggested that a rising plasma level of leucine is a physiologic stimulus for the release of insulin, and that the more pronounced sensitivity to leucine hypoglycemia produced experimentally by. administration of sulfonylureas and observed in some patients with idiopathic hypoglycemia or insulin-secreting tumors of the pancreas represents a great exaggeration of a normal physiologic phenomenon (6, 7).In an effort to determine the effect of leucine on insulin release under physiologic circumstances, protein meals rich in leucine were fed to healthy subjects, and the levels of plasma insulin, leucine, amino nitrogen, free fatty acids, and blood glucose

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