In T2DM, the expansion of visceral adipose tissue constitutes a persistent source of inflammatory signals mediated by cytokines (TNF-α, IL-6), chemokines (MCP-1), and dysfunctional adipokines (resistin, RBP4), which interfere with insulin signaling and sustain a state of systemic metaflammation [36]. Here, INS is linked to type 2 diabetes mellitus.