Hyperinsulinemia-induced excess insulin activity caused by insulin administration promotes vascular inflammation by producing proinflammatory cytokines in vascular smooth muscle cells.51 It is also noteworthy that TA-1887 treatment decreased levels of Icam-1, but not of Vcam-1, while insulin treatment had the opposite effect, increasing Vcam-1 but not Icam-1 levels (Fig. 4e, 6f). Here, ICAM1 is linked to Hyperinsulinemia.