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Am J Physiol Regul Integr Comp Physiol 262: R574-R578, 1992;
0363-6119/92 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 262, Issue 4 574-R578, Copyright © 1992 by American Physiological Society

ARTICLES

Satiety induced by endogenous and exogenous cholecystokinin is mediated by CCK-A receptors in mice

S. C. Weatherford, F. Y. Chiruzzo and W. B. Laughton
Department of Neurobiology and Obesity Research, Hoffmann-La Roche, Nutley, New Jersey 07110.

To investigate the relative participation of peripheral (CCK-A) and central (CCK-B) cholecystokinin (CCK) receptors in satiety induced by endogenous CCK, we examined the effect of the CCK-A antagonist MK-329 (10-315 micrograms/kg) and the CCK-B antagonist L 365260 (0.1-315 micrograms/kg) on intake of a 20% sucrose solution in mildly food-deprived mice. Intraperitoneal injection of MK-329 elicited a dose-related increase in sucrose consumption with a minimal effective dose of 31.5 micrograms/kg. This dose increased sucrose intake 23% and the highest dose tested, 315 micrograms/kg, increased sucrose intake 63% above baseline. In contrast to MK-329, intraperitoneal administration of L 365260 had no effect on sucrose intake at doses up to 315 micrograms/kg. To examine the contribution of these two CCK receptor subtypes in satiety induced by exogenous CCK, CCK-8 (8 micrograms/kg) was administered alone and in combination with MK-329 and L 365260. MK-329 (10 micrograms/kg) significantly attenuated the satiety effect of CCK-8, and L 365260 (100 micrograms/kg) was without effect. These results suggest that the peripheral CCK receptor subtype mediates satiety induced by endogenous and exogenous CCK in the mouse.


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