In parallel, recent studies have shown that obesity-related cadiometabolic risk can be mediated by the pleiotropic effects of adipokines, the secretory products that reflect endocrine function in adipose tissue [18], particularly by these adipokines which may function via the central nervous system (CNS), such as leptin, adiponectin, resistin, fibroblast growth factor 21 (FGF21) [19] and retinol binding protein 4 (RBP4) [20]. This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.