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APPETITE, OBESITY AND METABOLISM

Effects of peripheral CCK receptor blockade on food intake in rats

¹Department of Veterans Affairs Nebraska Western Iowa Health Care System, Omaha 68105; and Departments of ²Biomedical Sciences and ³Chemistry, Creighton University, Omaha, Nebraska 68178

Submitted 3 April 2003 ; accepted in final form 2 May 2003

Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated, in part, by CCK action at CCKARs located peripheral to the blood-brain barrier. At dark onset, non-food-deprived rats received a bolus injection of devazepide (2.5 µmol/kg iv), a 3-h infusion of A-70104 (1 or 3 µmol·kg^-1·h^-1 iv), or vehicle either alone or coadministered with a 3-h infusion of CCK-8 (10 nmol·kg^-1·h^-1 iv) or a 2-h intragastric infusion of peptone (1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of N-3-quinolinoyl-D-Glu-N,N-dipentylamide (A-65186), does not. CCK-8 inhibited 3-h food intake by more than 50% and both A-70104 and devazepide abolished this response. A-70104 and devazepide stimulated food intake and similarly attenuated the anorexic response to intragastric infusion of peptone. Thus endogenous CCK appears to act, in part, at CCKARs peripheral to the blood-brain barrier to inhibit food intake.

receptor antagonist; devazepide; A-70104; satiety

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