Overall, AT contributes to the development of obesity-induced inflammation by increasing cytokines and chemokines and dysregulation of adipokines such as TNF-ɑ, IL-6, IL-8, IL-1, monocyte chemoattractant protein-1 (MCP-1), leptin, PAI-1, retinol-binding protein 4 (RBP4), chemerin, serum amyloid A (SSA), C-reactive protein (CRP), lipopolysaccharide-binding protein (LBP), fetuin-A, and decreased adiponectin and omentin-1 (27). This evidence concerns the gene AHSG and obesity due to melanocortin 4 receptor deficiency.