Role of gastric distention in cholecystokinin's satiety effect in golden hamsters.

Cholecystokinin (CCK) inhibits gastric emptying in a number of species. Since gastric distention is facilitated by reduced gastric emptying, and since gastric distention is a long-known satiety stimulus, it is possible that CCK suppresses feeding by facilitating gastric distention satiety mechanisms. In the first experiment peripheral injections of CCK-octapeptide (CCK-8) inhibited gastric emptying in hamsters. The effective dose range corresponded to the dose range previously shown to be effective at inhibiting feeding in hungry hamsters. In a second experiment the sham-feeding paradigm, in which orally ingested liquid diet passes out of a gastric fistula (thereby eliminating gastric distention), was used to determine whether CCK-8 would reduce hamster feeding in the absence of gastric distention. An intraperitoneal dose of CCK-8 produced a slight and statistically unreliable suppression of sham-feeding. In contrast, the same dose produced a robust and reliable inhibition of feeding during a real-feeding trial (the gastric fistula was closed and the stomach was thus able to distend). These data therefore suggest that enhanced gastric distention may contribute to or magnify the satiety effect of peripherally administered CCK in this species. A third experiment examined the mechanism of CCK action on gastric emptying and feeding. Since (in other species) CCK appears to reduce the rate of gastric emptying primarily by constricting the pyloric sphincter, it was predicted that destroying pyloric control of gastric emptying by pyloroplasty would attenuate CCK's effect on both gastric clearance and feeding. However, pyloroplasty did not alter the normal inhibition of gastric emptying nor the usual feeding inhibitory response after a given dose of CCK-8.(ABSTRACT TRUNCATED AT 250 WORDS)