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Cell Metab. 2008 Oct;8(4):281-288. doi: 10.1016/j.cmet.2008.08.005.

The lipid messenger OEA links dietary fat intake to satiety.

Author information

1
Diabetes Research Center, Departments of Medicine and Neuroscience, Albert Einstein College of Medicine of Yeshiva University, Bronx, NY.
2
Department of Pharmacology, University of California, Irvine, California.
3
Department of Human Physiology and Pharmacology, University of Rome 'La Sapienza', Rome, Italy.
4
Unit of Drug Discovery and Development, Italian Institute of Technology, Genoa, Italy.
#
Contributed equally

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-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.

PMID:
18840358
PMCID:
PMC2572640
DOI:
10.1016/j.cmet.2008.08.005
[Indexed for MEDLINE]
Free PMC Article

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