The OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in mice.
Details
Serval ID
serval:BIB_FAC91FA69C28
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in mice.
Journal
Metabolism
ISSN
1532-8600 (Electronic)
ISSN-L
0026-0495
Publication state
Published
Issued date
10/2018
Peer-reviewed
Oui
Volume
87
Pages
13-17
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Abstract
Oleoylethanolamide (OEA) is an endocannabinoid that controls food intake, energy expenditure and locomotor activity. Its anorexigenic effect appears to be mediated by PPARα, but the tissue where the presence of this receptor is required for OEA to inhibit feeding is unknown as yet. Previous studies point to a possible role of proximal enterocytes and neurons of the nodose ganglion.
Acute intraperitoneal OEA effects on food intake, energy expenditure, respiratory exchange ratio (RER) and locomotor activity were studied in control mice (PPARα-loxP) and intestinal (Villin-Cre;PPARα-loxP) or nodose ganglion (Phox2B-Cre;PPARα-loxP) specific PPARα knockout mice placed in calorimetric cages.
OEA administration to both intestinal and nodose ganglion PPARα knockout mice decreased food intake, RER (leading to increased lipid oxidation) and locomotor activity as in control mice. However, while OEA injection acutely decreased energy expenditure in controls, this effect was not observed in mice devoid of PPARα in the intestine.
These results indicate that the OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in the intestine.
Acute intraperitoneal OEA effects on food intake, energy expenditure, respiratory exchange ratio (RER) and locomotor activity were studied in control mice (PPARα-loxP) and intestinal (Villin-Cre;PPARα-loxP) or nodose ganglion (Phox2B-Cre;PPARα-loxP) specific PPARα knockout mice placed in calorimetric cages.
OEA administration to both intestinal and nodose ganglion PPARα knockout mice decreased food intake, RER (leading to increased lipid oxidation) and locomotor activity as in control mice. However, while OEA injection acutely decreased energy expenditure in controls, this effect was not observed in mice devoid of PPARα in the intestine.
These results indicate that the OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in the intestine.
Keywords
Animals, Eating/drug effects, Endocannabinoids/pharmacology, Energy Metabolism/drug effects, Intestinal Mucosa/drug effects, Intestinal Mucosa/metabolism, Intestines/drug effects, Lipid Metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Activity/drug effects, Nodose Ganglion/drug effects, Nodose Ganglion/metabolism, Oleic Acids/pharmacology, PPAR alpha/drug effects, PPAR alpha/genetics, PPAR alpha/metabolism, Endocannabinoid, Energy expenditure, Food intake, OEA
Pubmed
Web of science
Create date
29/06/2018 17:41
Last modification date
20/08/2019 17:26
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