CCKA receptor-deficient mice and rats 31,65, PrRP-deficient mice 18 and oxytocin receptor-deficient mice 66 (Fig. 7) all show an increased meal size and late-onset obesity, suggesting the importance of the CCK–PrRP–oxytocin pathway in the control of food intake, especially in the termination of each meal. This evidence concerns the gene CCK and obesity disorder.