Abstract

Recent evidence indicates that endogenous opiate peptides may be involved in the control of food intake. In previous experiments, injection of β-endorphin has stimulated food intake and peripheral injections of the opiate antagonist, naloxone, decreased food intake in rats. In the present experiments, food and water intakes of sheep were measured in response to peripherally administered opiate antagonists and continuous lateral ventricular administration of opiate agonists. Intravenous injections of both of the opiate antagonists naloxone (0.03, 0.062 and 0.125 mg/kg) and 3–4(hydroxyl-phenyl)-3-4-dimethyl-piperidine propiophenone maleate (0.03, 0.062 and 0.125 mg/kg) decreased food intake for up to 90 min in 4-hr fasted sheep. In water-deprived sheep, naloxone did not affect water intake or body temperature for the first 4 hr but depressed 24 hr water intake. Continuous 90-min injection of 26, 51 and 102 nmoles/min of the opiate agonist D-ala 2-met-enkephalinamide (DME) increased food intake of satiated sheep. Intravenous injection of 0.125 mg/kg naloxone blocked the increase in food intake elicited by intraventricular injection of DME. In contrast, intraventricular injection of kyotorphin, a releasor of endogenous enkephalin in the brain, did not affect food intake. Thus, in sheep intracerebroventricular administration of opiate agonists increased food intake; peripheral administration of opiate antagonists decreased food intake and blocked the feeding induced by agonists.

Full Text
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