CCK-receptor antagonists attenuate suppression of sham feeding by intestinal nutrients

• Published in: The American journal of physiology Vol. 262; no. 4 Pt 2; p. R554
• Main Authors: Yox, D P, Brenner, L, Ritter, R C
• Format: Journal Article
• Language: English
• Published: United States 01.04.1992
• Subjects: Amylases - metabolism; Animal Nutritional Physiological Phenomena; Animals; Benzodiazepinones - pharmacology; Catheterization; Cholecystokinin - antagonists & inhibitors; Cholecystokinin - blood; Devazepide; Duodenum - enzymology; Eating - drug effects; Intestines - physiology; Male; Maltose - pharmacology; Oleic Acid; Oleic Acids - pharmacology; Phenylalanine - pharmacology; Proglumide - analogs & derivatives; Proglumide - antagonists & inhibitors; Proglumide - pharmacology; Rats; Rats, Inbred Strains; Receptors, Cholecystokinin - antagonists & inhibitors; Satiety Response - physiology; Sincalide - pharmacology; Stomach
• ISSN: 0002-9513
• DOI: 10.1152/ajpregu.1992.262.4.r554

To test the possibility that endogenous cholecystokinin (CCK) participates in suppression of sham feeding by intraintestinal nutrient infusions, we examined the effect of CCK-receptor antagonists on the suppression of sham feeding by intraintestinally infused oleic acid, maltose or L-phenylalanine (L-Phe). In addition, we monitored amylase activity in the intestinal lumen during some sham feeding experiments and measured plasma CCK in parallel experiments using intestinally infused animals that were not feeding. Suppression of sham feeding by oleic acid or maltose was attenuated by CCK-receptor antagonists, while suppression of sham feeding by L-Phe was not. Oleate infusion increased plasma CCK concentration and luminal amylase activity. Oleate-induced increase in luminal amylase activity was attenuated by a CCK-receptor antagonist. Intraintestinal maltose or L-Phe did not increase plasma CCK concentration or luminal amylase activity, suggesting that they did not release endocrine CCK. These results suggest 1) that endogenous CCK mediates suppression of sham feeding by oleate and maltose but not by L-Phe and 2) that CCK participating in suppression of feeding by intestinal stimuli might not be of endocrine origin.