Role of cholecystokinin in the anorexia produced by duodenal delivery of peptone in rats

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1999-06, Vol.276 (6), p.R1701
• Main Authors: Woltman, Todd, Reidelberger, Roger
• Format: Article
• Language: English
• ISSN: 1522-1490
• DOI: 10.1152/ajpregu.1999.276.6.R1701

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.