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. Author manuscript; available in PMC: 2014 Jan 8.
Published in final edited form as: Cell Metab. 2013 Jan 8;17(1):20–33. doi: 10.1016/j.cmet.2012.11.012

Fig. 5. Selective insulin resistance in vascular cells in type 2 diabetes.

Fig. 5

Schematic illustration of mechanisms causing impaired insulin signaling in vascular endothelial and smooth muscle cells. ET-1, angiotensin II, and other factors can be increased by the metabolic milieu and activate PKC. Activated PKC, in turn, can phosphorylate IRS proteins, the p85 subunit of PI3K, and other signaling molecules. In this state, insulin-stimulated activation of the PI3K signaling is inhibited while signaling through the MAPK pathway is preserved or enhanced. Selective insulin resistance in vascular cells cause impaired vasodilation and angiogenesis, reduced antioxidant effects and increased leukocyte adhesion. Abbreviations (see also fig. 3): eNOS, endothelial nitric oxide synthase; ET-1, endothelin-1; FFA, free fatty acids; HO-1, heme oxygenase-1; INSR, insulin receptor; IRS, insulin receptor substrate; TNF-α, tumor necrosis factor-α; VCAM-1, vascular cell adhesion molecule-1. Artwork by Leah A. Klein.