AJP - Gastrointestinal and Liver Physiology, Vol 249, Issue 6 733-G738, Copyright © 1985 by American Physiological Society
Cholecystokinin is not a peripheral satiety signal in the dog
T. N. Pappas, R. L. Melendez, K. M. Strah and H. T. Debas
The doses of cholecystokinin (CCK) that have been shown to cause satiety
after peripheral administration are pharmacological and whether
"physiological" doses of exogenous CCK or endogenously released CCK have a
satiety effect is not known. The purpose of the present study is threefold:
to compare the potency of endogenous and exogenous CCK for their satiety,
cholecystokinetic, and pancreozyminic actions; to determine whether small
doses of CCK in the presence of gastric distension cause satiety; and to
test the satiety effect of CCK administered centrally into the lateral
cerebral ventricle. Dogs were prepared with cerebroventricular guides and
esophageal and duodenal fistulas (n = 4), with chronic bile fistulas (n =
8), and chronic pancreatic fistulas (n = 7). Satiety effect was quantified
in the esophageal fistula dog by the amount of blenderized food sham fed
within 7.5 min. Duodenal perfusion of fat, used as a releaser of endogenous
CCK, stimulated pancreatic protein, and gallbladder contraction with D50
values of 1.5 and 0.3 mmol/h, respectively, but had no effect on the volume
sham fed (316 +/- 82 ml/min without and 371 +/- 41 ml/min with the maximal
dose of sodium oleate infused). The D50 values of CCK-8 (pmol X kg-1 X h-1)
for satiety and for stimulation of pancreatic enzyme secretion and
gallbladder contraction were 440, 120, and 22, respectively. Injection of
CCK-8 into the lateral cerebral ventricle inhibited sham feeding in a
dose-dependent manner. We conclude that duodenal fat in doses producing
maximal gallbladder and pancreatic stimulation has no satiety effect in the
dog.(ABSTRACT TRUNCATED AT 250 WORDS)
