Gastric control of food intake

Inhibition of gastric emptying leads to enhanced satiety and this mechanism may contribute to the undereating observed after administration of cholecystokinin (CCK) and fenfluramine, and in patients with anorexia nervosa. Pyloric smooth muscle bears specific CCK receptors and the evidence suggests that a major site of action for CCK satiety is in the periphery. CCK receptors are widespread in the neonatal rat stomach but not in the brain and over the first two weeks of life binding in the stomach decreases and that in the brain increases. This and the finding that independent ingestion as well as gastric emptying are inhibited by CCK at birth suggest the stomach as its likely site of action in the neonatal rat. Fenfluramine inhibits feeding in animals and in patients with bulimia nervosa. In monkeys, fenfluramine inhibits gastric emptying and this action correlates with its feeding inhibition. Patients with anorexia nervosa who are acutely starving and rats maintained on a restricted diet have delayed gastric emptying. Anorexic patients showed abnormal reporting of both hunger and satiety, and, together with those with bulimia nervosa, often associated gastric contents with symptoms of eating disorder, indicating disturbed interpretation of gastric signals.