The development of dual agonists for the glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide receptor (GLP-1R and GIPR respectively) is a landmark moment in the treatment of type 2 diabetes and obesity. In preclinical and clinical studies, GLP-1R-GIPR co-agonism improves glycemia and reduces body weight superior to GLP-1R agonism alone, however the location and role of GIPR activation remains incompletely understood. Evidence suggests that long acting GIPR agonists act in the CNS to reduce food intake and body weight via an inhibitory GABAergic neuronal population. Here we demonstrate that acyl-GIP decreases food intake in lean mice but not in mice with deletion of GIPR in the area postrema, a component of the hindbrain’s dorsal vagal complex (DVC), which lies at the caudal end of the brainstem and integrates sensory information from the gastrointestinal tract, controls food intake and aversive responses. Furthermore, we demonstrate this population is responsible for alleviating the avoidance response, a proxi for an antiemetic action in mice, to PYY by acyl-GIP. Our data demonstrate that long acting GIPR agonists depend on GIPR signalling in the area postrema to decrease food intake and body weight.