While hypothalamic POMC deficiency may result in improved glucose tolerance, treatment with setmelanotide should, in theory, have the opposite effect; however, setmelanotide did not result in a significant worsening of glucose metabolism parameters in individuals with POMC or LEPR deficiency.78 Indeed, setmelanotide was associated with a significant improvement in fasting glucose values in patients with POMC; however, this was not the case for LEPR deficiency. This evidence concerns the gene POMC and obesity due to pro-opiomelanocortin deficiency.