Abstract Hypoglycemia can induce hunger, but evidence of increased rates of glucose utilization contributing to satiety signals is tenuous. Therefore, monkeys (4.5–6.5 kg) were given 30-min injections of 0.9% NaCl on control days or glucose (5 g) into the jugular vein, mesentary vein, or stomach prior to daily 2-hr feedings. In spite of high levels of serum glucose, immunoreactive insulin and glucose utilization rate prior to and during initial stages of the feeding period, food intake was essentially not decreased. A similar pre-feeding load of 25 g into the stomach was also ineffective. However, if 25 g were given during the first 30 min of the feeding, the monkeys ate very little after 30 min, total depression, 60 per cent. Thus, high levels of glucose and glucose utilization alone are not sufficiently strong satiety factors in monkeys to reduce food intake of a single daily meal. However, if gastrointestinal glucose loads accompany oral feeding, intake of a scheduled meal is greatly suppressed. It is not clear what mechanism sensitizes the satiety receptor system to these signals of glucose metabolism.