Increased food intake after type A but not type B cholecystokinin receptor blockade

RL Corwin, J Gibbs, GP Smith - Physiology & behavior, 1991 - Elsevier
RL Corwin, J Gibbs, GP Smith
Physiology & behavior, 1991Elsevier
To assess the role of cholecystokinin (CCK) receptors in mediating the satiating effect of an
oral preload, overnight food-deprived rats (n= 7) were given access to a high-carbohydrate
liquid diet for 40 min. At the end of 40 min, food was removed and rats were injected
subcutaneously (SC) with devazepide (DVZ; 1 ng/kg-1 mg/kg), an antagonist selective for
the CCK-A receptor, or its vehicle, 0.5% carboxymethylcellulose (CMC). Thirty min after
injection, rats were given access to the same liquid food for 60 min. DVZ increased food …
To assess the role of cholecystokinin (CCK) receptors in mediating the satiating effect of an oral preload, overnight food-deprived rats (n=7) were given access to a high-carbohydrate liquid diet for 40 min. At the end of 40 min, food was removed and rats were injected subcutaneously (SC) with devazepide (DVZ; 1 ng/kg-1 mg/kg), an antagonist selective for the CCK-A receptor, or its vehicle, 0.5% carboxymethylcellulose (CMC). Thirty min after injection, rats were given access to the same liquid food for 60 min. DVZ increased food intake significantly. Furthermore, the effectiveness of a very low dose of DVZ (10 ng/kg) is strong evidence that the effect of DVZ was specific for CCK-A receptors. Three of the rats that increased food intake after DVZ were also tested with L-365,260, an antagonist selective for the CCK-B receptor (10 ng/kg-100 μg/kg). L365,260 did not increase food intake significantly. These results confirm and extend previous reports that CCK-A receptor blockade increases food intake after an oral preload. They do not, however, demonstrate a role for the CCK-B receptor in mediating the satiating effect of ingested food under the same experimental conditions.
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