AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 3 620-R624, Copyright © 1993 by American Physiological Society
Blockade of type A, but not type B, CCK receptors postpones satiety in rhesus monkeys
T. H. Moran, P. J. Ameglio, H. J. Peyton, G. J. Schwartz and P. R. McHugh
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
The exogenous administration of the brain/gut peptide cholecystokinin (CCK)
inhibits food intake in a variety of species, including subhuman primates
and humans. To determine the role of endogenously released CCK in the
control of food intake in rhesus monkeys, we examined the ability of the
selective type A and type B CCK antagonists devazepide and L-365260 to
affect total daily food intake and various meal patterns. Various doses of
the antagonists were administered intragastrically 30 min before a daily
4-h feeding period. One-gram food pellets were delivered in response to
lever pulls, and intake was computer monitored. Intragastric administration
of the type A CCK receptor antagonist devazepide (10-320 micrograms/kg)
significantly increased food intake in a dose-related fashion. The
threshold for increasing intake was 32 micrograms/kg, and a maximal effect
was obtained at a dose of 100 micrograms/kg that increased total 4-h food
intake by 47%. The effect of devazepide on food intake was mediated by
significant increases in the size and duration of the initial meal,
lengthening of the subsequent intermeal interval, and a decrease in the
satiety ratio (intermeal interval/1st meal size). In contrast, intragastric
administration of the type B CCK receptor antagonist L-365260 (3.2-320
micrograms/kg) did not significantly affect total food intake or any of the
meal parameters. These data demonstrate that endogenously released CCK
acting through type A CCK receptors plays a role in regulating food intake
in rhesus monkeys.
