Given that pro-inflammatory cytokines and chemokines, like tumor necrosis factor alfa (TNF-α), interleukin-6 (IL-6) and resistin, overproduced by the dysfunctional adipose tissue in obesity, can activate intracellular pathways that trigger IR in insulin-target tissues [15], the anti-inflammatory potential of PUFAs may indirectly improve the peripheral insulin responsiveness, reducing the risk of glyco-metabolic alterations in patients with IR [49]. Here, IL6 is linked to obesity due to melanocortin 4 receptor deficiency.