Obesity is a chronic disease linked to increased risks of type 2 diabetes, cardiovascular disorders, and metabolic dysfunction. As global obesity rates continue to rise, bariatric surgery, particularly Roux-en-Y gastric bypass (RYGB), has become a well-established intervention for achieving sustained weight loss and improving obesity-related comorbidities. Cholecystokinin (CCK) is a gut hormone released by enteroendocrine cells in response to food intake. It plays a key role in appetite regulation, promoting satiety, slowing gastric emptying, and stimulating digestive enzyme secretion. Acting through CCK1 receptors and signaling via the vagus nerve, CCK has been shown to reduce food intake in various experimental models. This study focuses on evaluating hormonal changes following RYGB, with an emphasis on the role of CCK. While research findings vary—due to differences in sample timing, patient variability, and methodologies—evidence supports the involvement of CCK in the improved satiety observed after surgery. Factors such as diet composition, meal timing, and individual health status significantly influence CCK response. The findings suggest that CCK contributes to the metabolic benefits of RYGB and may serve as a potential target for therapeutic interventions in obesity treatment. However, further standardized, well- controlled studies are needed to clarify its mechanisms and interactions with other gut hormones.