In individuals with MetS, hypertrophy and dysfunction of visceral adipose tissue promote the secretion of a broad spectrum of bioactive mediators, including pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), adipokines—most notably leptin and adiponectin—and pro-atherogenic molecules [37,38]. Here, TNF is linked to metabolic syndrome.