Mechanisms of oleoylethanolamide-induced changes in feeding behavior and motor activity.

Karine Proulx, Daniela Cota, Tamara R. Castañeda, Matthias H. Tschöp, David A. D'Alessio, Patrick Tso, Stephen C. Woods, Randy J. Seeley
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2005-09-01; 289(3): R729-R737
DOI: 10.1152/ajpregu.00029.2005

PubMed
Lire sur PubMed



1. Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R729-37. Epub 2005 May 5.

Mechanisms of oleoylethanolamide-induced changes in feeding behavior and motor
activity.

Proulx K(1), Cota D, Castañeda TR, Tschöp MH, D’Alessio DA, Tso P, Woods SC,
Seeley RJ.

Author information:
(1)Genome Research Institute, ML 0506, University of Cincinnati, 2170 E.
Galbraith Road, Cincinnati, OH 45237, USA.

Oleoylethanolamide (OEA), a lipid synthesized in the intestine, reduces food
intake and stimulates lipolysis through peroxisome proliferator-activated
receptor-alpha. OEA also activates transient receptor potential vanilloid type 1
(TRPV1) in vitro. Because the anorexigenic effect of OEA is associated with
delayed feeding onset and reduced locomotion, we examined whether intraperitoneal
administration of OEA results in nonspecific behavioral effects that contribute
to the anorexia in rats. Moreover, we determined whether circulating levels of
other gut hormones are modulated by OEA and whether CCK is involved in
OEA-induced anorexia. Our results indicate that OEA reduces food intake without
causing a conditioned taste aversion or reducing sodium appetite. It also failed
to induce a conditioned place aversion. However, OEA induced changes in posture
and reduced spontaneous activity in the open field. This likely underlies the
reduced heat expenditure and sodium consumption observed after OEA injection,
which disappeared within 1 h. The effects of OEA on motor activity were similar
to those of the TRPV1 agonist capsaicin and were also observed with the
peroxisome proliferator-activated receptor-alpha agonist Wy-14643. Plasma levels
of ghrelin, peptide YY, glucagon-like peptide 1, and apolipoprotein A-IV were not
changed by OEA. Finally, antagonism of CCK-1 receptors did not affect OEA-induced
anorexia. These results suggest that OEA suppresses feeding without causing
visceral illness and that neither ghrelin, peptide YY, glucagon-like peptide 1,
apolipoprotein A-IV, nor CCK plays a critical role in this effect. Despite that
OEA-induced anorexia is unlikely to be due to impaired motor activity, our data
raise a cautionary note in how specific behavioral and metabolic effects of OEA
should be interpreted.

DOI: 10.1152/ajpregu.00029.2005
PMID: 15879057 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus