TY - JOUR
T1 - Effects of peripheral CCK receptor blockade on food intake in rats
AU - Reidelberger, Roger D.
AU - Castellanos, Daniel A.
AU - Hulce, Martin
PY - 2003/8/1
Y1 - 2003/8/1
N2 - 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
α-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.
AB - 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
α-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.
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U2 - 10.1152/ajpregu.00176.2003
DO - 10.1152/ajpregu.00176.2003
M3 - Article
C2 - 12738611
AN - SCOPUS:0041808024
VL - 285
SP - R429-R437
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
SN - 0363-6119
IS - 2 54-2
ER -