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 | |
| State | Published - Oct 8 2008 |
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Keywords
- HUMDISEASE
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Physiology
Cite this
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 journal › Article
}
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 -