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Am J Physiol Regul Integr Comp Physiol 271: R1521-R1528, 1996;
0363-6119/96 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 6 1521-R1528, Copyright © 1996 by American Physiological Society


ARTICLES

Role of cholecystokinin in the anorexia produced by duodenal delivery of glucose in rats

T. Woltman and R. Reidelberger
Veterans Affairs Medical Center, Omaha, Nebraska 68105, USA.

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, and 18.3 mmol.kg-1.h-1) and the glucose dimer maltose (4.5, 6.7, and 8.5 mmol.kg-1.h-1) at the start of the dark period in nonfasted 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-1.h-1 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-1.h-1). 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.


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