OXT and morbid obesity: Notably, the attenuative effect of OXT signaling on larval zebrafish feeding behavior is consistent with mammalian studies: (1) the insatiable appetite and morbid obesity observed in Prader–Willi syndrome is likely due to impaired OXT signaling53,54; (2) acute inhibition of paraventricular OXT neurons can promote food intake55; (3) lesions of the PVN, as well as mutations that affected OXT neuron development, have been shown to cause hyperphagia and obesity56,57; and (4) direct administration of OXT has been shown to reduce feeding4,5.