Mechanistically, increased TSH levels in subclinical hypothyroidism promoted the secretion of cytokines IL-1α, IL-1β and IL-6 by inducing macrophage M1 polarization, which upregulated EGR1 to transcriptionally activate LCN2 and SOCS3 in insulin target cells, thereby exacerbating insulin resistance. Here, LCN2 is linked to Insulin resistance.