However, arteries isolated from VAT of obese CD36 KO mice showed a complete and significant recovery of the dilatory response to flow (∼85% of baseline at maximum flow) as compared to VAT arteries from obese WT mice and similar to that observed in arteries of lean WT mice (Fig. 4), thereby supporting a role for CD36 in obesity-induced endothelial dysfunction in VAT arteries. This evidence concerns the gene CD36 and obesity due to melanocortin 4 receptor deficiency.