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AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 5 1001-R1005, Copyright © 1993 by American Physiological Society
ARTICLES |
K. McHugh, T. W. Castonguay, S. M. Collins and H. P. Weingarten
Intestinal Disease Research Unit, McMaster University, Hamilton, Ontario, Canada.
Experimental colitis was induced in rats by intrarectal infusion of trinitrobenzenesulfonic acid and ethanol. Colitis was accompanied by a large suppression of food intake of 3 days duration. The reduction of food intake was effected through a reduction of meal size, with no change in meal frequency. Those same rats demonstrating approximately 70%-80% suppression of daily food intake showed no reduction of sham feeding. These data indicate that malaise alone is inadequate to explain the suppression of food intake associated with acute colitis. Rather, the data suggest that the suppression of eating results from an exaggerated postprandial satiety signal elaborated during the period of acute inflammation, an interpretation consistent with the demonstration of a slowed rate of gastric emptying in association with the colitis.
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