Together, these findings point to a role for a CD36-mediated FA uptake mechanism initiated by VAT that results in the impairment of Kir2.1, prompting further investigation into a VAT/FA/CD36/Kir2.1 axis as a contributor to obesity-endothelial dysfunction. This evidence concerns the gene KCNJ2 and obesity due to melanocortin 4 receptor deficiency.