Brainstem-restricted receptor for GDF15 which regulates food intake, energy expenditure and body weight in response to metabolic and toxin-induced stresses (PubMed:28953886, PubMed:28846099, PubMed:28846097, PubMed:28846098). Upon interaction with its ligand, GDF15, interacts with RET and induces cellular signaling through activation of MAPK- and AKT- signaling pathways (PubMed:28846098, PubMed:28846099). Interacts (via the extracellular domain) with GDF15 and RET; receptor of GDF15, mediates cellular signaling through interaction with RET after GDF15-binding (PubMed:28846098, PubMed:28846099). Interaction with RET requires previous GDF15-binding (PubMed:28846099). Expressed in the brainstem, restricted to cells in the area postrema and the immediately adjacent region of the nucleus tractus solitarius. On a chow diet, mutants show no difference in food intake, energy expenditure or body weight compare to wild-type controls. On high-fat diet, they gain substantially more weight and are more glucose intolerant. Diet-induced obese mutants are hyperphagic and have 32% greater total mass and 9% greater lean mass than diet-induced obese wild-type mice (PubMed:28953886, PubMed:28846097, PubMed:28846099). Upon chronical administration of GDF15, mutants are refractory to the GDF15 effects in comparison to wild-types that show attenuated food-intake and sustained weightloss (PubMed:28846098, PubMed:28953886, PubMed:28846097, PubMed:28846099). Belongs to the GDNFR family.