Insulin resistance reduces arterial prostacyclin synthase and eNOS activities by increasing endothelial fatty acid oxidation
J. Clin. Invest. Xueliang Du, et al. 116:1071 doi:10.1172/JCI23354 [Go to this article.]

Figure 1
Schematic mechanism by which IR causes increased oxidation of FFA in arterial endothelial cells, activating proatherogenic signals and inhibiting antiatherogenic enzymes. IR, insulin resistance; ACC, acetyl-CoA carboxylase; CPT-I, carnitine palmitoyltransferase I; AGE, advanced glycation end product; GlcNAc, N-acetylglucosamine; PGI₂, prostacyclin.