CCK-A receptor antagonists have selective effects on nutrient-induced food intake suppression in rats.

To provide additional support to the hypothesis that only dietary protein (Pro; chicken egg albumin) and not amino acids (AA; patterned after albumin), carbohydrates (CHO; cornstarch), or fats (Fat; corn oil) produces a satiating effect via CCK receptors, two CCK-A receptor antagonists (PD-140,548 and devazepide) were coadministered with each nutrient. Given alone [4 ml intragastrically (ig)] Pro (1.0 g), AA (1.0 g), CHO (1.4 g), and Fat (2.4 g) suppressed (P < 0.05) food intake on average during the first 2 h of feeding by 1.4 (36%), 1.5 (48%), 1.0 (33%), and 1.2 g (41%), respectively. Devazepide (0.5 mg/kg) and PD-140,548 (1.0 mg/kg) given alone increased food intake during 0-2 h by 0.7 g (18%) and during 0-1 h by 0.5 g (15%), respectively. When coadministered with PD-140,548 (1.0 mg/kg ip), the suppression of food intake caused by Pro was modulated during 0-2 h by 57% (Pro x drug interaction, P < 0.05), but AA-, CHO-, and Fat-induced suppression of feeding was not affected (nutrient x drug interaction, P > 0.05). Devazepide (0.5 mg/kg ip) did not modulate AA-, CHO-, and Fat-induced food intake suppression during any time period (nutrient x drug interaction, P > 0.05). These studies provide additional evidence that CCK-A receptors play a role in Pro (albumin) but not AA-, CHO (cornstarch)-, or Fat (corn oil)-induced food intake suppression in rats.

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 albumin) and not amino acids (AA), carbohydrates (CHO; cornstarch), or fats (Fat; corn oil) produces a satiating effect via cholecystokinin (CCK) receptors, devazepide was coadministered with each macronutrient. Given 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; and 1.0 g, respectively, and in the first 2 h of feeding by 0.8, 1.2, and 1.3 g; 1.7 g; 0.7 g; and 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, and 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 intraperitoneally also modulated Pro intake suppression during the first hour by 33% and during 0-2 h by 79%. Devazepide appears to interact with mechanisms of Pro-induced food intake suppression, but not AA-, Fat-, or CHO-induced food intake suppression. These studies provide evidence that CCK receptors play a role in Pro (albumin)- but not AA-, CHO (corn starch)-, or Fat (corn oil)-induced food intake suppression in rats.

Effects of essential amino acids on food and water intake of rats.

This study examined the effects of selected groups of essential amino acids (EAAs), given by gavage, on short-term food and water intake. Amino acid groups were selected on the basis of their common physiologic functions in relation to current hypotheses on the role of amino acids in food intake control, and the quantities given were based on the proportions in 1.5 g of the EAA content of albumin. The complete EAA mixture (1.5 g) suppressed food intake by an average of 60 and 37% during the 1st and 2nd h of feeding, respectively, but had no influence on feeding in the subsequent 12 h. Total daily (14 h) intake was decreased by 9%. With the exception of the aromatic amino acid (Phe + Tyr + Trp, 0.34 g) group, all groups significantly decreased food intake by a comparable magnitude (32%) during the 1st h. In this time period, rats given the EAAs, Arg + Met + Val (0.38 g), and Arg + His + Lys (0.44 g) mixtures increased their water intake, whereas intake by rats given the Phe + Tyr + Trp + Thr (0.46 g) and Ile + Leu + Val (0.45 g) mixtures was unchanged. Thus, the food intake suppression caused by EAAs was not accounted for by an equal effect of its component amino acid groups. As well, food intake suppression by amino acid groups was not explained by increased water consumption, nor was it simply related to the quantity of nitrogen provided by the treatment.