Oleoylethanolamide (OEA), a lipid synthesized in the intestine, reduces food intake and stimulates lipolysis through peroxisome proliferator-activated receptor-alpha (PPAR-α). 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 ip administration of OEA results in non-specific 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 cholecystokinin (CCK) is involved in OEAinduced 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 hour. The effects of OEA on motor activity were similar to those of the TRPV1 agonist capsaicin, and were also observed with the PPAR-α agonist Wy-14643. Plasma levels of ghrelin, peptide YY (PYY), glucagon-like peptide 1 (GLP-1) and apolipoprotein A-IV (apo 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, PYY, GLP-1, apo A-IV nor CCK play 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.