In line with FMD and MPO measurements obtained from bariatric patients, organ bath experiments confirmed obesity-induced endothelial dysfunction to be attenuated dramatically in Mpo−/− mice in both obesity models, indicating that this effect is for the most part independent of altered leptin signaling in Lep−/− mice (Figures 2F and 2G). This evidence concerns the gene MPO and obesity due to melanocortin 4 receptor deficiency.