The pathophysiological interplay remains incompletely elucidated, but several mechanistic hypotheses have been proposed: Chronic inflammatory-driven pathway: Proinflammatory cytokines in psoriasis (e.g., TNF-α, IL-6, IL-17) systematically induce insulin resistance through suppression of insulin receptor substrates and impairment of glucose uptake in adipose tissue (10). This evidence concerns the gene TNF and psoriasis.