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

Research output: Contribution to journalArticle

235 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)281-288
Number of pages8
JournalCell Metabolism
Volume8
Issue number4
DOIs
StatePublished - Oct 8 2008

Fingerprint

Dietary Fats
Fats
Lipids
Peroxisome Proliferator-Activated Receptors
Oleic Acid
Satiety Response
CD36 Antigens
Small Intestine
Meals
Obesity
Eating
Carbohydrates
oleoylethanolamide
Membranes
Pharmaceutical Preparations
Proteins

Keywords

  • HUMDISEASE

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Physiology

Cite this

Schwartz, G. J., Fu, J., Astarita, G., Li, X., Gaetani, S., Campolongo, P., ... Piomelli, D. (2008). The Lipid Messenger OEA Links Dietary Fat Intake to Satiety. Cell Metabolism, 8(4), 281-288. https://doi.org/10.1016/j.cmet.2008.08.005

The Lipid Messenger OEA Links Dietary Fat Intake to Satiety. / Schwartz, Gary J.; Fu, Jin; Astarita, Giuseppe; Li, Xiaosong; Gaetani, Silvana; Campolongo, Patrizia; Cuomo, Vincenzo; Piomelli, Daniele.

In: Cell Metabolism, Vol. 8, No. 4, 08.10.2008, p. 281-288.

Research output: Contribution to journalArticle

Schwartz, GJ, Fu, J, Astarita, G, Li, X, Gaetani, S, Campolongo, P, Cuomo, V & Piomelli, D 2008, 'The Lipid Messenger OEA Links Dietary Fat Intake to Satiety', Cell Metabolism, vol. 8, no. 4, pp. 281-288. https://doi.org/10.1016/j.cmet.2008.08.005
Schwartz GJ, Fu J, Astarita G, Li X, Gaetani S, Campolongo P et al. The Lipid Messenger OEA Links Dietary Fat Intake to Satiety. Cell Metabolism. 2008 Oct 8;8(4):281-288. https://doi.org/10.1016/j.cmet.2008.08.005
Schwartz, Gary J. ; Fu, Jin ; Astarita, Giuseppe ; Li, Xiaosong ; Gaetani, Silvana ; Campolongo, Patrizia ; Cuomo, Vincenzo ; Piomelli, Daniele. / The Lipid Messenger OEA Links Dietary Fat Intake to Satiety. In: Cell Metabolism. 2008 ; Vol. 8, No. 4. pp. 281-288.
@article{9398733bed784465a2173cd1da53eea9,
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.",
keywords = "HUMDISEASE",
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",
year = "2008",
month = "10",
day = "8",
doi = "10.1016/j.cmet.2008.08.005",
language = "English (US)",
volume = "8",
pages = "281--288",
journal = "Cell Metabolism",
issn = "1550-4131",
publisher = "Cell Press",
number = "4",

}

TY - JOUR

T1 - The Lipid Messenger OEA Links Dietary Fat Intake to Satiety

AU - Schwartz, Gary J.

AU - Fu, Jin

AU - Astarita, Giuseppe

AU - Li, Xiaosong

AU - Gaetani, Silvana

AU - Campolongo, Patrizia

AU - Cuomo, Vincenzo

AU - Piomelli, Daniele

PY - 2008/10/8

Y1 - 2008/10/8

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.

KW - HUMDISEASE

UR - http://www.scopus.com/inward/record.url?scp=52749087007&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=52749087007&partnerID=8YFLogxK

U2 - 10.1016/j.cmet.2008.08.005

DO - 10.1016/j.cmet.2008.08.005

M3 - Article

C2 - 18840358

AN - SCOPUS:52749087007

VL - 8

SP - 281

EP - 288

JO - Cell Metabolism

JF - Cell Metabolism

SN - 1550-4131

IS - 4

ER -