Endogenous cholecystokinin and intestinal satiety.
The role of endogenous cholecystokinin (CCK) as a mediator of intestinal satiety is examined. We used rats equipped with a chronic gastric fistula and an indwelling duodenal catheter to assess the effects of direct duodenal stimulation on sham feeding. To evaluate the contribution of endogenous CCK to intestinal satiety we used a specific competitive antagonist of the satiety action of CCK, proglumide. Intraduodenal infusion of 11 or 5 ml liquid diet suppressed sham feeding. Administration of proglumide caused a partial reversal of the suppression of feeding produced by the 11-ml, but not the 5-ml, intraduodenal infusion. Administration of proglumide alone did not influence sham feeding but completely abolished the suppression of sham feeding induced by a maximal dose of exogenous CCK. These results indicate that CCK contributes to intestinal satiety under specific test conditions only. Moreover, since that component of suppression reversed by proglumide was small in comparison with the overall inhibition of eating, these results indicate that factors other than CCK are important in intestinal satiety.
D000704:Analysis of Variance; D000818:Animals; D001066:Appetite / Q000502:physiology*; D002408:Catheters, Indwelling; D002766:Cholecystokinin / Q000502:physiology*; D004386:Duodenum; D005526:Food, Formulated; D008297:Male; D010649:Phenylalanine / Q000494:pharmacology; D011377:Proglumide / Q000494:pharmacology; D051381:Rats; D012844:Sincalide / Q000494:pharmacology; D013997:Time Factors
D010649:Phenylalanine; D002766:Cholecystokinin; D011377:Proglumide; D012844:Sincalide