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Although the exact mechanisms that contribute to diabetic complications remain unclear, it has recently been suggested that disequilibrium between toxic metabolites (e.g., advanced glycation end-products, protein kinase C activation), oxidative stress, and protective endogenous factors (e.g., insulin, vascular endothelial growth factor, platelet-derived growth factors, and adiponectin) may play a role in diabetic complications (Jeong and King, 2011)