Peripheral cholecystokinin (CCK) is thought to inhibit food intake by activating CCK-A receptors at a gastric and/or vagal afferent site.' If this effect persists after gastrectomy, then peripheral extragastric CCK receptor sites that regulate food intake might exist. The aims of our study were to determine: (1) if exogenous CCK inhibits food intake after gastrectomy in rats; (2) if blockade of endogenous CCK increases food intake and body weight after total gastrectomy in rats; and (3) which CCK receptor subtypes (CCK-A or CCK-B) are involved.
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