These include autoxidation, non-enzymatic glycation of proteins due to extended exposure to hyperglycaemia, metabolism of glucose via aldose reductase with changes in sorbitol-myoinositol concentrations and the increased de novo synthesis of diacylglycerol from glycolytic intermediates and subsequent activation of the protein kinase C pathway [43,44]. This evidence concerns the gene AKR1B1 and Hyperglycemia.