2008
DOI: 10.1016/j.cmet.2008.08.005
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The Lipid Messenger OEA Links Dietary Fat Intake to Satiety

Abstract: Summary The association between fat consumption and obesity underscores the need to identify physiological signals that control fat intake. Previous studies have shown that feeding stimulates small-intestinal mucosal cells to produce the lipid messenger oleoylethanolamide (OEA) which, when administered as a drug, decreases meal frequency by engaging peroxisome proliferator-activated receptors-α (PPAR-α). Here we report that duodenal infusion of fat stimulates OEA mobilization in the proximal small intestine, w… Show more

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Cited by 317 publications
(380 citation statements)
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“…As confirmation of this possibility, the pharmacological administration of OEA in experimental animals regulates satiety and reduces body weight by reducing the frequency of meals by activating the nuclear receptor PPAR-alpha (peroxisome proliferator-activated receptor alpha), which has been involved in a feedback mechanism involving recruitment, utilization, and absorption of dietary fat [108,110,111]. According to some authors, the mechanism of action of OEA in regulating appetite in response to the introduction of food, after activating the intestinal receptor PPAR-alpha, consists in the involvement of vagal sensory fibers that carry a stimulus to the first nucleus tractus solitaire (NST) at the base of the brain, and thus the paraventricular nucleus of the hypothalamus (PVH), resulting in the sense of satiety by blockade, a mechanism that can be defined as feedback through food intake (Fig.…”
Section: Sense Of Satietymentioning
confidence: 99%
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“…As confirmation of this possibility, the pharmacological administration of OEA in experimental animals regulates satiety and reduces body weight by reducing the frequency of meals by activating the nuclear receptor PPAR-alpha (peroxisome proliferator-activated receptor alpha), which has been involved in a feedback mechanism involving recruitment, utilization, and absorption of dietary fat [108,110,111]. According to some authors, the mechanism of action of OEA in regulating appetite in response to the introduction of food, after activating the intestinal receptor PPAR-alpha, consists in the involvement of vagal sensory fibers that carry a stimulus to the first nucleus tractus solitaire (NST) at the base of the brain, and thus the paraventricular nucleus of the hypothalamus (PVH), resulting in the sense of satiety by blockade, a mechanism that can be defined as feedback through food intake (Fig.…”
Section: Sense Of Satietymentioning
confidence: 99%
“…In fact, studies in experimental animals on the metabolism of oleic acid in the intestine suggest that activation of smallintestinal OEA mobilization, enabled by CD36-mediated uptake of dietary oleic acid, serves as a molecular sensor linking fat ingestion to satiety [103][104][105][106][107][108]. OEA, a lipidderived molecule with endogenous hormone-like action is formed, which is structurally similar to the endocannabinoid anandamide (arachidonoiletanolamide).…”
Section: Sense Of Satietymentioning
confidence: 99%
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“…CD36 is expressed in the brush border of duodenal and jejunal epithelia. CD36-KO mice have reduced OEA production and OEA-induced satiety [73], the latter of which can be induced via PPARα activation [73,74].…”
Section: Gastrointestinal Lipid Sensingmentioning
confidence: 99%