Background: Exogenous oxytocin (OT) reduces reward-driven food intake. Less is known about endogenous OT and eating behaviour. Preclinical studies suggest peripheral OT levels may reflect the opposite of central appetite-related OT activity. In healthy females, circulating OT declines after eating. Whether this pattern exists in obesity and how endogenous OT relates to hedonic eating remains unclear. We hypothesised that OT would decrease postprandially in adults with obesity and that higher OT exposure, reflecting lower central OT signalling, would correlate with greater reward-driven caloric intake. Methods: Sixty-one adults with obesity (56% female; age [mean ± SE] 33.55 ± 0.81 years; BMI 36.77 ± 0.62 kg/m²) consumed a standardised meal following an overnight fast. OT was measured in peripheral blood pre-meal and 30, 60, and 120 min post-meal. Area under the curve (AUC) was calculated to capture OT exposure. Postprandial hedonic eating drive was assessed via visual analogue scales (VAS) and Cookie Taste Test (CTT). Meal-related OT dynamics were analysed using linear mixed effects models, relationships between OT exposure and hedonic eating drive were examined with linear regression and mediation analyses. Results: OT levels did not change in response to the meal. Greater OT AUC was associated with reduced postprandial satisfaction (p = 0.008, d = 1.00) and higher CTT caloric intake (p = 0.036, d = 0.62). The relationship between OT AUC and CTT caloric intake was mediated by OT's effect on postprandial satisfaction (p = 0.014, proportion mediated = 53.28%). Conclusions: In obesity, OT levels did not change postprandially. Greater OT exposure was linked to lower satisfaction and increased hedonic eating, suggesting dysregulated OT signalling in obesity potentially contributing to overeating.