Evidence of the endogenous oxytocinergic dysfunction that leads to impaired satiety and obesity is well-established in persons with Prader–Willi syndrome [271,272], who had a reduced number and size of oxytocin-producing parvocellular neurons that are associated with a reduction in oxytocin secretion [273]. This evidence concerns the gene OXT and obesity due to melanocortin 4 receptor deficiency.