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. Author manuscript; available in PMC: 2014 Nov 21.
Published in final edited form as: Rev Endocr Metab Disord. 2008 Dec;9(4):301–314. doi: 10.1007/s11154-008-9104-2

Figure 2. Schematic of Hyperglycemic Effects on Biochemical Pathways in Diabetic Neuropathy [49].

Figure 2

Excessive glucose metabolism generates excess NADH and leads to overload of the electron transport chain causing oxidative stress, damage to Mt, activation of PARP. PARP activation by ROS acts in conjunction with the hexosamine and PKC pathway to induce inflammation and neuronal dysfunction. A combination of oxidative stress and hyperglycemia activate the detrimental pathways of AGE, polyol, hexosamine and PKC pathways which lead to redox imbalance, gene expression disturbances, and further oxidative stress. These pathways also induce inflammation and neuronal dysfunction. Abbreviations: NF-κB, Nuclear factor kappa B; PARP, Poly(ADP-ribose) polymerase; PKC, Protein kinase C; AGE, Advanced glycation endproducts; RNS, Reactive nitrogen species; ROS, Reactive oxygen species, GSH, glutathione; GSSG, oxidized glutathione; UDPGlcNAc, UDP-N-Acetylglucosamine; VEGF, Vascular endothelial growth factor. (Reprinted from Pharmacol Ther. 2008 Jun 13. Diabetic neuropathy: Mechanisms to management, Edwards JL, Vincent AM, Cheng HL, Feldman EL Copy right 2008 with permission form Elsevier).