Role of cholecystokinin in the anorexia produced by duodenal delivery of peptone in rats
Woltman, T.; Reidelberger, R.
American Journal of Physiology 276(6): R1701-R1709
1999
ISSN/ISBN: 0002-9513 PMID: 10362750 Document Number: 507950
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 mg/kg) stimulated food intake dose dependently by 30-73%, with a minimal effective dose of 100 mg/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 mg/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 mg/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. Reprinted by permission of the publisher.