The Lipid Messenger OEA Links Dietary Fat Intake to Satiety

Gary J. Schwartz; Jin Fu; Giuseppe Astarita; Xiaosong Li; Silvana Gaetani; Patrizia Campolongo; Vincenzo Cuomo; Daniele Piomelli

doi:10.1016/j.cmet.2008.08.005

The Lipid Messenger OEA Links Dietary Fat Intake to Satiety

Gary J. Schwartz, Jin Fu, Giuseppe Astarita, Xiaosong Li, Silvana Gaetani, Patrizia Campolongo, Vincenzo Cuomo, Daniele Piomelli

Medicine

Research output: Contribution to journal › Article › peer-review

262 Scopus citations

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)
Pages (from-to)	281-288
Number of pages	8
Journal	Cell metabolism
Volume	8
Issue number	4
DOIs	https://doi.org/10.1016/j.cmet.2008.08.005
State	Published - Oct 8 2008

Keywords

HUMDISEASE

ASJC Scopus subject areas

Physiology
Molecular Biology
Cell Biology

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10.1016/j.cmet.2008.08.005

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title = "The Lipid Messenger OEA Links Dietary Fat Intake to Satiety",

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.",

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author = "Schwartz, {Gary J.} and Jin Fu and Giuseppe Astarita and Xiaosong Li and Silvana Gaetani and Patrizia Campolongo and Vincenzo Cuomo and Daniele Piomelli",

note = "Funding Information: We thank Dr. Viviana Trezza for help with the behavioral characterization of PPAR -α-null mice and Ms. Fariba Oveisi for help with other animal experiments. This study was supported by NIH DK073955 (D.P.), NIH DK047208 (G.J.S.), the Skirball Institute, the NY Obesity Research Center (NIH 5P30DK026687), and Italian Ministry of Research (PRIN 2007) (V.C.). ",

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AU - Schwartz, Gary J.

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AU - Gaetani, Silvana

AU - Campolongo, Patrizia

AU - Cuomo, Vincenzo

AU - Piomelli, Daniele

N1 - Funding Information: We thank Dr. Viviana Trezza for help with the behavioral characterization of PPAR -α-null mice and Ms. Fariba Oveisi for help with other animal experiments. This study was supported by NIH DK073955 (D.P.), NIH DK047208 (G.J.S.), the Skirball Institute, the NY Obesity Research Center (NIH 5P30DK026687), and Italian Ministry of Research (PRIN 2007) (V.C.).

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N2 - 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.

AB - 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.

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The Lipid Messenger OEA Links Dietary Fat Intake to Satiety

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