1. Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.145
Figure 4 Transendothelial transport of insulin in a skeletal muscle capillary
Figure 4 | Transendothelial transport of insulin in a skeletal muscle capillary. Insulin stimulates its own transendothelial transport by clathrin-dependent nitric oxide (NO)-mediated endocytosis and transcytosis. In skeletal muscle and in adipose tissue, the non-fenestrated microvascular endothelial monolayer forms a tight barrier that restricts free access of plasma constituents to the subendothelial interstitium and, if not activated, prevents interaction of blood cells with the endothelium. Insulin binds to the insulin receptor on the endothelial plasma membrane and the resulting complex is engulfed by clathrin-mediated endocytosis, transported through the endothelial cell and released by exocytosis. After passing through the basement membrane, insulin binds to its target cells and stimulates glucose uptake via facilitated glucose transporter member 4 (GLUT-4). Transcytosis of insulin is stimulated by NO, which is generated by insulin-stimulated activation of endothelial NO-synthase (eNOS). These insulin actions are impaired in patients with insulin resistance.
Artunc, F. et al. (2016) The impact of insulin resistance on the kidney and vasculature
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