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The ability of cholecystokinin (CCK) to act as a long-term satiety factor was assessed by its continuous infusion into the jugular veins of rats. Animals receiving a low dose of cholecystokinin octapeptide (CCK-8) (0.6 microgram CCK-8.kg body wt-1.h-1) did not show any significant differences in body weight changes or in food consumption from rats receiving saline and a group of unoperated controls over the 7-day infusion period. A 19.3-fold greater dose of CCK-8 (11.6 micrograms.kg body wt-1.h-1) did cause a significant decline in food consumption for the first 4 days compared with saline-infused rats (P less than 0.05) and unoperated controls (P less than 0.01). Rats receiving a high dose of CCK gained weight at a slower rate than rats receiving saline, but this effect lasted only 2 days and was not significant. Pancreatic growth was used as an indirect measure of elevated CCK levels in these animals. The infusion of 0.6 microgram CCK-8.kg body wt-1.h-1 did not lead to sufficiently elevated peptide levels to promote pancreatic growth. In contrast, those rats receiving a high dose of CCK-8 had significantly greater pancreatic weights (P less than 0.01) compared with saline-treated rats and unoperated controls. These results indicate that CCK-8, when administered continuously and in a large enough dose, can suppress food intake in rats for a period of several days before losing its effectiveness.

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This study demonstrates that for the isolated cat gall bladder a smaller molar dose of the sulfated form of OP-CCK and gastrin is required to produce contraction as compared to the respective non-sulfated forms. For OP the D50 for the sulfated form versus the non-sulfated form was 1.94. For gastrin it was 1.10.