Role of cholecystokinin in the anorexia produced by duodenal
delivery of glucose in rats.
Woltman, Todd, and Roger Reidelberger.
Veterans Administration Medical Center, Omaha, NE 68105 and
Department of Biomedical Sciences, Creighton University School of
Medicine, Omaha, NE 68178
APStracts 3:0219R, 1996.
We used the type A cholecystokinin receptor (CCK-AR) antagonist
devazepide to assess the importance of CCK in mediating the anorexia
produced by 2-h duodenal infusions of glucose (9.2, 11.0, 18.3
mmol/kg-h) and the glucose dimer maltose (4.5, 6.7, 8.5 mmol/kg-h) at
the start of the dark period in non-fasted rats with free access to
food. Glucose and maltose appeared to inhibit 2- to 3-h food intakes
dose-dependently from 19 to 91 %. The highest doses of glucose and
maltose administered suppressed feeding similarly by increasing first
meal latency and decreasing meal frequency; lower doses produced less
reliable effects on meal patterns. Devazepide appeared to completely
reverse the cumulative intake responses and some of the meal pattern
responses to the 9.2 mmol/kg-h dose of glucose, and to partially
attenuate responses to the two higher glucose doses and to the
minimal effective dose of maltose (6.7 mmol/kg-h). The magnitudes of
these devazepide effects were not statistically different from those
produced by devazepide when vehicle was infused duodenally. These
results suggest that CCK may play a significant, necessary role in
mediating the satiety response to duodenal delivery of small but not
large loads of glucose.
Received 10 July 1995; accepted in final form 23 May 1995.
APS Manuscript Number R429-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96