Abstract

The site where peripherally administered cholecystokinin-8 elicits satiety was investigated by injecting rats with cholecystokinin-8 (1 to 8 micrograms per kilogram of body weight, intraperitoneally) after they had received bilateral lesions of the ventromedial hypothalamus or after they had undergone bilateral abdominal vagotomy or selective vagotomies. Abdominal vagotomy or gastric vagotomy abolished or reduced the satiety effect of cholecystokinin, but lesions of the ventromedial hypothalamus did not. These results demonstrate that peripherally administered cholecystokinin acts in the abdomen through gastric vagal fibers and not directly on the brain to produce satiety in the rat.