Abstract
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, 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-α 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.
Original language | English (US) |
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Pages (from-to) | 281-288 |
Number of pages | 8 |
Journal | Cell metabolism |
Volume | 8 |
Issue number | 4 |
DOIs | |
State | Published - Oct 8 2008 |
Keywords
- HUMDISEASE
ASJC Scopus subject areas
- Physiology
- Molecular Biology
- Cell Biology