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Articles in PresS, published online ahead of print October 31, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00529.2002
Submitted on September 3, 2002
Accepted on October 18, 2002
1 Veterans Administration Medical Center, Omaha, NE, USA; Biomedical Sciences, Creighton University, Omaha, NE, USA
2 Biomedical Sciences, Creighton University, Omaha, NE, USA
3 Veterans Administration Medical Center, Omaha, NE, USA
4 Chemistry, Creighton University, Omaha, NE, USA
* To whom correspondence should be addressed. E-mail: rogerr{at}creighton.edu.
Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that duodenal delivery of protein, carbohydrate, and fat produce satiety in part by an essential CCK action at CCKARs located peripheral to the blood-brain barrier. Fasted rats with open gastric fistulas received devazepide (1 mg kg-1 IV) or A-70104 (700 nmol kg-1 h-1 IV) and either a 30 min IV infusion of CCK-8 (10 nmol kg-1 h-1) or duodenal infusion of peptone, maltose, or Intralipid beginning 10 min before 30-min access to 15% sucrose. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of Na-3-quinolinoyl-D-Glu-N,N-dipentylamide, does not. CCK-8 inhibited sham feeding by about 50% and both A-70104 and devazepide abolished this response. Duodenal infusion of each of the macronutrients dose-dependently inhibited sham feeding. A-70104 and devazepide attenuated inhibitory responses to each macronutrient. Thus, endogenous CCK appears to act in part at CCKARs peripheral to the blood-brain barrier to inhibit food intake.
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