PRRT2 and Hyperglycemia: On the other hand, the hyperglycemia-induced tissue injury has been shown to be mediated by the following mechanisms, including the increased flux of glucose and other sugars through the polyol pathway, the increased production of advanced glycation end products (AGEs), activation of protein kinase C (PKC) isoforms, increased hexosamine pathway flux and consequent over-modification of proteins by N-acetylglucosamine, and these pathways are all activated by the hyperglycemia-induced mitochondrial superoxide production by inhibiting GAPDH [6].