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Recent incretin\u2010based and multi\u2010agonist therapies have delivered unprecedented weight loss, demonstrating that the simultaneous modulation of multiple metabolic pathways can optimize body weight control and improve obesity\u2010related comorbidities. However, biological heterogeneity, interindividual variability in treatment response and uncertainties regarding long\u2010term outcomes highlight the need to explore complementary regulatory mechanisms. Oleoylethanolamide (OEA) is an endogenous lipid mediator synthesized on demand in the small intestine in response to dietary lipid intake. Acting primarily through peroxisome proliferator\u2010activated receptor\u2010\u03b1 (PPAR\u2010\u03b1), OEA functions as a physiological satiety signal that promotes fatty acid oxidation and coordinates gut\u2013brain communication. Preclinical evidence indicates that OEA reduces food intake without inducing malaise, enhances lipid utilization and improves metabolic dysfunction in models of diet\u2010induced obesity, while engaging both homeostatic and reward\u2010related neural circuits. Emerging clinical studies report modest but consistent effects on body weight and selected cardiometabolic parameters. 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