Hedonic eating refers to the consumption of food uniquely because of its </div><div>gustatory rewarding properties and not for homeostatic needs; so the subject eats also when not in a </div><div>state of energy depletion. Hedonic eating may stimulate powerfully food intake; hence, </div><div>understanding its physiological modulation could improve our knowledge of the pathophysiology of </div><div>obesity. Furthermore, obese people often present binge-eating behaviours, and binge-eating is </div><div>experienced as rewarding. Endocannabinoids, including anandamide (AEA) and 2-</div><div>arachidonoylglycerol (2-AG), and endocannabinoid-related compounds, oleoylethanolamide (OEA) </div><div>and palmitoylethanolamide (PEA), are involved in the modulation of food-related reward. </div><div>

Therefore, in the present study we aimed to investigate the responses </div><div>of endocannabinoids and endocannabinoid-related compounds to hedonic eating in obese patients </div><div>with and without binge eating disorder (BED). </div><div>

Peripheral levels of AEA, 2-AG, OEA and PEA were measured in 7 obese patients </div><div>with BED and 7 obese patients without BED after eating hedonic and non-hedonic food, and </div><div>compared to those of normal weight healthy controls. </div><div>

Peripheral levels of endocannabinoids and endocannabinoid-related compounds </div><div>exhibited different response patterns to hedonic eating among the groups. </div><div>

These data confirm the role of endocannabinoids and endocannabinoid-related </div><div>compounds in food-related reward and suggest a dysregulation of their physiology in obesity and in </div><div>the BED. These findings may have potential relevance to the prevention and treatment of obesity </div><div>and BED.</div>