Abstract
Oleoylethanolamide (OEA) is an endogenous lipid that contributes in important ways to the peripheral regulation of food intake. When administered intraperitoneally, OEA is a potent satiety-inducing anorexiant in rats and mice [Nature 414 (2001) 209; Neuropsycopharmacology 28 (2003) 1311; Nature 425 (2003) 90]. In the present study, we show that oral administration of OEA in pH-sensitive enteric-coated capsules produces a profound and long-lasting inhibition of food intake in free-feeding rats. This effect is accompanied by a marked elevation in OEA levels in the small intestine, but not in brain or muscle.
Highlights
Oleoylethanolamide (OEA) is an endogenous lipid mediator that participates in the control of feeding behavior
The main finding of this study is that oral administration of OEA to free-feeding rats causes a persistent inhibition of food intake, demonstrating that this compound is an orally active anorexiant
A similar inhibition was obtained with a four-fold lower dose when OEA was administered in capsules coated with a gastroprotected pH-sensitive resin
Summary
Oleoylethanolamide (OEA) is an endogenous lipid mediator that participates in the control of feeding behavior. OEA is potent at decreasing food intake in rats and mice [1,2,3]. This effect is due to a selective change in the onset and frequency of feeding—a strong indication of increased satiety—and is not accompanied by aversive or stress-related responses [1,2]. The anorexiant effect of OEA is mediated by visceral sensory fibers of the vagus nerve, and is accompanied by activation of brain structures—nucleus of the solitary tract, hypothalamic paraventricular nucleus—that are intimately involved in the control of energy balance [1]. As a result of PPAR-␣ activation, OEA produces satiety, and reduces
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