EFFECT OF A CHOLECYSTOKININ-A RECEPTOR BLOCKER ON PROTEIN-INDUCED FOOD-INTAKE SUPPRESSION IN RATS

To test the hypothesis that only dietary protein (Pro; chicken egg alb umin) and not amino acids (AA), carbohydrates (CHO; cornstarch), or fa ts (Fat; corn oil) produces a satiating effect via cholecystokinin (CC K) receptors, devazepide was coadministered with each macronutrient. G iven alone (in 4 ml ig), Pro (0.75, 1.0, and 1.5 g), AA (1.0 g), CHO ( 1.4 g), and Fat (2.4 g) suppressed (P < 0.05) food intake in the first hour by 0.5, 0.8, and 1.1 g; 1.9 g; 1.9 g; and 1.0 g, respectively, a nd in the first 2 h of feeding by 0.8, 1.2, and 1.3 g; 1.7 g; 0.7 g; a nd 1.5 g, respectively. When coadministered with devazepide (0.5 mg/kg body wt ig), the suppression of food intake caused by Pro, AA, CHO, a nd Fat treatments was modulated in the first hour by 60, 50, and 55%; 16%, 11%; and 10%, respectively, and during 0-2 h by 63, 92, and 54%; 29%; 0%; and -20%, respectively. Devazepide (0.5 mg/kg) given intraper itoneally also modulated Pro intake suppression during the first hour by 33% and during 0-2 h by 79%. Devazepide appears to interact with me chanisms of Pro-induced food intake suppression, but not AA-, Fat-, or CHO-induced food intake suppression. These studies provide evidence t hat CCK receptors play a role in Pro (albumin)- but not AA-, CHO (corn starch)-, or Fat (corn oil)-induced food intake suppression in rats.