these considerations suggest that future efforts should be directed toward developing agents that increase early but not late postprandial plasma insulin concentrations and that restore a normal postprandial pattern of glucagon secretion. Agents that facilitate the suppression of hepatic glucose release and the stimulation of glucose uptake by insulin and glucose may also be of value. It is doubtful, however, that such agents will fully normalize postprandial carbohydrate metabolism without increasing the risk of hypoglycemia unless they also restore the dynamic interaction of glucose, insulin, and glucagon