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Veterans Administration Medical Center, Omaha 68105; and Department of Biomedical Sciences, Creighton University School of Medicine, Omaha, Nebraska 68178
We used the cholecystokinin receptor
antagonist devazepide to assess the importance of CCK in mediating the
anorexia produced by 2-h duodenal infusions of peptone, a protein
digest, at dark onset in nonfasted rats. Peptone alone (0.14-2.24
g/h) suppressed food intake dose dependently by 18-96%, with an
approximate half-maximal dose of 1 g/h. Peptone-induced reductions in
caloric ingestion were comparable to the caloric loads infused.
Devazepide alone (30-1,000 µg/kg) stimulated food intake dose
dependently by 30-73%, with a minimal effective dose of 100 µg/kg. Devazepide appeared to reverse the anorexic response to
peptone (1.1 g/h) dose dependently by 29-65%, with a minimal
effective dose of 30 µg/kg. The magnitudes of these
devazepide-induced effects were similar to, and in some cases were
larger than, those produced when the same doses of devazepide were
administered alone. Coadministration of devazepide (1,000 µg/kg) and
a lower peptone dose (0.8 g/h) produced similar results. These results
suggest that an essential CCK mechanism plays a significant role in
mediating the satiety response to duodenal delivery of protein.
meal patterns; satiety; protein; cholecystokinin receptor antagonist; devazepide
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