Accordingly, in isolated mouse aortas and mouse aortic endothelial cells, omentin was shown to protect against vascular-endothelial dysfunction induced by high glucose through the inhibition of endoplasmic reticulum and oxidative stress and by increasing NO production via activation of AMPK/peroxisome proliferator-activated receptor δ (PPARδ) pathway [303]. The gene discussed is ITLN1; the disease is endothelial dysfunction.