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CCK-receptor antagonists attenuate suppression of sham feeding by intestinal nutrients
D P Yox1, L Brenner, R C Ritter
1Department of Veterinary and Comparative Anatomy, College of Veterinary Medicine, Washington State University, Pullman 99164-6520.
Abstract:
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.
Insights
Endogenous cholecystokinin (CCK) suppresses sham feeding induced by oleic acid and maltose, but not L-phenylalanine. This CCK may not originate from endocrine sources.
Area of Science:
- Gastroenterology
- Neuroscience
- Physiology
Background:
- Intraintestinal nutrient infusions are known to suppress feeding behavior.
- Endogenous cholecystokinin (CCK) is a peptide hormone implicated in satiety signaling.
- The precise role of CCK in nutrient-induced feeding suppression requires further elucidation.
Purpose of the Study:
- To investigate the role of endogenous cholecystokinin (CCK) in the suppression of sham feeding by intraintestinal nutrient infusions.
- To determine if CCK receptor antagonists affect the feeding suppressive effects of oleic acid, maltose, and L-phenylalanine.
- To assess the origin of CCK involved in feeding suppression.
Main Methods:
- Sham feeding experiments were conducted with intraintestinal infusions of oleic acid, maltose, or L-phenylalanine.
- CCK-receptor antagonists were administered to assess their effect on feeding suppression.
- Intestinal luminal amylase activity and plasma CCK levels were measured.
- Experiments were performed in animals that were not feeding to measure plasma CCK.
Main Results:
- CCK-receptor antagonists attenuated the suppression of sham feeding by oleic acid and maltose.
- L-phenylalanine did not suppress sham feeding, even with CCK-receptor antagonists.
- Oleic acid infusion increased plasma CCK and luminal amylase activity, an effect blunted by CCK-receptor antagonists.
- Maltose and L-phenylalanine did not increase plasma CCK or luminal amylase activity.
Conclusions:
- Endogenous CCK mediates the suppression of sham feeding induced by oleic acid and maltose.
- CCK does not appear to mediate feeding suppression by L-phenylalanine.
- The CCK involved in suppressing feeding by intestinal stimuli may not be of endocrine origin.