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

Aurélie Caillon; Kalina Duszka; Walter Wahli; Françoise Rohner-Jeanrenaud; Jordi Altirriba

doi:10.1016/j.metabol.2018.06.005

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

Metabolism. 2018 Oct:87:13-17. doi: 10.1016/j.metabol.2018.06.005. Epub 2018 Jun 21.

Authors

Aurélie Caillon¹, Kalina Duszka², Walter Wahli³, Françoise Rohner-Jeanrenaud¹, Jordi Altirriba⁴

Affiliations

¹ Laboratory of Metabolism, Department of Medicine Specialties, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
² Center for Integrative Genomics, University of Lausanne, Le Génopode, 1015 Lausanne, Switzerland.
³ Center for Integrative Genomics, University of Lausanne, Le Génopode, 1015 Lausanne, Switzerland; Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, 11 Mandalay Road, 308232, Singapore.
⁴ Laboratory of Metabolism, Department of Medicine Specialties, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, Switzerland. Electronic address: [email protected].

PMID: 29936173
DOI: 10.1016/j.metabol.2018.06.005

Abstract

Background: 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.

Materials and methods: 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.

Results: 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.

Conclusion: 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: Endocannabinoid; Energy expenditure; Food intake; OEA.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

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*

Substances

Endocannabinoids
Oleic Acids
PPAR alpha
oleoylethanolamide