| Literature DB >> 18840358 |
Jin Fu1, Giuseppe Astarita1, Gary J Schwartz2, Xiaosong Li2, Silvana Gaetani3, Patrizia Campolongo3, Vincenzo Cuomo3, Daniele Piomelli1,4.
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.Entities:
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Year: 2008 PMID： 18840358 PMCID： PMC2572640 DOI： 10.1016/j.cmet.2008.08.005
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287