Role of cholecystokinin in the anorexia produced by duodenal
delivery of oleic acid in rats.
Woltman, Todd, Daniel Castellanos, and Roger Reidelberger.
Veterans Administration Medical Center, Omaha, NE 68105 and
Department of Biomedical Sciences, Creighton University School of
Medicine, Omaha, NE 68178
APStracts 2:0193R, 1995.
To assess the importance of triglyceride digestion products in
producing satiety, we determined the effects of duodenal infusions of
triolein, oleic acid, and oleic acid plus monoolein on meal patterns
in ad libitum feeding rats. Oleic acid and oleic acid plus monoolein
inhibited feeding similarly; triolein's effect was delayed and 4-fold
less potent. We then used the CCKA receptor antagonist devazepide to
assess the importance of CCK in mediating the anorexia produced by
oleic acid. Oleic acid (320, 440, 640 [mu]mol/h) inhibited 3-h intake
dose-dependently by 32, 56, and 75%. Devazepide (1 or 2 mg/kg)
blocked the responses to the 320 [mu]mol/h dose, but had little if
any effect on responses to the larger doses. Devazepide (1 mg/kg) did
block anorexic responses to 3-h CCK-8 infusions (3, 10 nmol/kg-h IV)
that inhibited 3-h intake by 25 and 65%. Our results suggest that the
satiety response to triolein is produced by the products of triolein
digestion, and that CCK plays a significant indispensable role in
mediating the satiety response to duodenal delivery of small but not
large loads of oleic acid.
Received 28 October 1994; accepted in final form 23 June 1995.
APS Manuscript Number R625-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.