LEP and endothelial dysfunction: In vitro studies showed that leptin activates the AKT/GSK3β/β-catenin pathway, increasing the levels of ICAM (intercellular adhesion molecule)-1 and VCAM (vascular cell adhesion molecule)-1 and the rearrangement of the cytoskeleton, which results in increased endothelial cell migration and enhanced monolayer permeability, thus, favoring endothelial dysfunction [104].