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The lipid messenger OEA links dietary fat intake to satiety
Authors: Schwartz GJ, Fu J, Astarita G, Li X, Gaetani S, Campolongo P, Cuomo V, Piomelli D
- Journals: Cell Metab, Pecans
- Pages: 281-8
- Volume: Oct.;8(4)
- Year: 2008
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-alpha (PPAR-alpha). Here; we report that duodenal infusion of fat stimulates OEA mobilization in the proximal small intestine; whereas infusion of protein or carbohydrate does not. OEA production utilizes dietary oleic acid as a substrate and is disrupted in mutant mice lacking the membrane fatty-acid transporter CD36. Targeted disruption of CD36 or PPAR-alpha abrogates the satiety response induced by fat. The results suggest that activation of small-intestinal OEA mobilization; enabled by CD36-mediated uptake of dietary oleic acid; serves as a molecular sensor linking fat ingestion to satiety.