Gut peptides and food in the gut produce similar satiety effects.

We compared the satiety effects and mechanisms of action of food stimuli delivered to anatomically restricted areas of the gut with the satiety effects and mechanisms of action of the gut peptides cholecystokinin (CCK) and bombesin (BBS). When food is limited to contact with the pregastric and gastric gut surfaces at a test meal, rats stop eating and display the fixed sequence of postprandial behaviors which characterizes normal satiety. This "gastric satiety" effect is unaffected by total abdominal vagotomy. Intraperitoneal administration of BBS produces a large, specific, and dose-related inhibition of food intake at a test meal; this action, like the gastric satiety effect of food, is unaffected by total abdominal vagotomy. Since a BBS-like peptide is present in high concentration in the stomach, these parallels between gastric satiety and BBS-induced satiety suggest that an endogenous BBS-like peptide plays a role in gastric satiety. When small amounts of food are infused directly into the small intestine of sham feeding rats, they stop eating and display the behavioral satiety sequence. This "intestinal satiety" effect requires the synergistic input of oropharyngeal food stimulation in close temporal association. Intraperitoneal administration of CCK alone to sham feeding rats stops eating and elicits the behavioral satiety sequence; this action, like the intestinal satiety effect of food, requires the synergistic input of oropharyngeal food stimulation in close temporal association. Since CCK is present in high concentration in the upper small intestine, and is released into the circulation by food at this site, the parallels between intestinal satiety and CCK-induced satiety suggest that endogenous CCK plays a role in intestinal satiety.