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AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 4 946-R950, Copyright © 1990 by American Physiological Society
ARTICLES |
M. A. Della-Fera, C. A. Baile, B. D. Coleman, J. L. Miner and J. A. Paterson
Department of Internal Medicine, Washington University School of Medicine, St. Louis 63110.
Signals from the gastrointestinal (GI) tract, arising during ingestion and digestion of food, are important in the termination of feeding. This study was carried out to determine whether the satiety triggered by specific GI stimuli in sheep could be reversed by central nervous system (CNS) administration of dynorphin, a putative endogenous kappa-opiate receptor ligand, which has been shown to be a potent feed-intake stimulant in many species. Rumen distension and increased intraruminal concentration of propionic acid (an energy substrate produced during fermentation in the rumen) both significantly decreased feed intake in fasted sheep. When either of these stimuli were combined with continuous 60-min lateral cerebroventricular injection of [D-Ala2]dynorphin A-(1-13) (0.32 nmol/min), feed intake returned to control levels. Increasing feed intake in food-producing animals is an important way of improving production efficiency. The findings of these experiments illustrate how manipulation of a CNS opioid system can modify the effects of feed intake-limiting factors generated by ingestion of a meal, thereby promoting greater feed intake.
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