This could be secondary to a hyperglycemia-induced increase in polyol pathway activity, as SGCs are the major site of aldose reductase expression in DRG [82], thereby providing a mechanism by which aldose reductase inhibition was effective in restoring IGF-1 expression and release in DRG of diabetic rodents and cells exposed to hyperglycemia. Here, AKR1B1 is linked to Hyperglycemia.