Binge eating disorder (BED) and obesity are complex diseases characterized by maladaptive feeding behaviors, particularly towards palatable foods. The mesocorticolimbic dopamine system, also known as the "reward system," plays a crucial role in hedonic food intake and is implicated in both disorders. The endocannabinoid system (ECS), present in the reward system, regulates feeding behaviors but its involvement in BED and obesity is not fully elucidated. Recent research suggests its significant role in feeding behaviors, especially in addictive-like eating behaviors, prompting the hypothesis of common ECS regulations in these disorders.To test this hypothesis, adult male Wistar rats were subjected to BED and obesity models. Rats were exposed either to a 6-week continuous (obesity model) or intermittent (binge eating disorder model) diet with a free choice access to fat and to a 10% sucrose solution (fcHFHS). Bingeing behavior was assessed as significantly higher sucrose/fat intake during the first hour of access in the intermittent, compared with the continuous access group. ECS gene expression was evaluated in cortical, striatal, and mesencephalic brain regions using qPCR after diet exposure.Results revealed differential regulation of ECS genes based on the schedule of palatable food access, indicating distinct impacts of binge eating behavior and obesity on ECS gene expression within the reward system. Moreover, correlation analysis demonstrated that the macronutrient profile of highly consumed food can influence ECS gene expression. These findings enhance our understanding of ECS molecular adaptation in BED and obesity models, potentially aiding in the identification of new ECS targets for therapy.