The Lipid Messenger OEA Links Dietary Fat Intake to Satiety

被引：289

作者：

Schwartz, Gary J. ^{[2
,3
]}

Fu, Jin ^{[1
]}

Astarita, Giuseppe ^{[1
]}

Li, Xiaosong ^{[2
,3
]}

Gaetani, Silvana ^{[4
]}

Campolongo, Patrizia ^{[4
]}

Cuomo, Vincenzo ^{[4
]}

Piomelli, Daniele ^{[1
,5
]}

机构：

[1] Univ Calif Irvine, Dept Pharmacol, Irvine, CA 92717 USA

[2] Yeshiva Univ, Albert Einstein Coll Med, Diabet Res Ctr, Dept Med, Bronx, NY USA

[3] Yeshiva Univ, Albert Einstein Coll Med, Diabet Res Ctr, Dept Neurosci, Bronx, NY USA

[4] Univ Roma La Sapienza, Dept Physiol & Pharmacol, Rome, Italy

[5] Italian Inst Technol, Unit Drug Discovery & Dev, Genoa, Italy

来源：

CELL METABOLISM | 2008年 / 8卷 / 04期

关键词：

D O I：

10.1016/j.cmet.2008.08.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：281 / 288

页数：8

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