“…Therefore, it is important to find medical options other than glycemic control to prevent diabetic ocular complications. The metabolic changes that accompany hyperglycemia, such as activation of the polyol pathway (Gabbay, 1973;Lorenzi, 2007;Robison et al, 1988;, activation of protein kinase C (PKC) (Frank, 2002;Liang et al, 2005;Shiba et al, 1993), increased oxidative stress (Gurler et al, 2000;Jennings et al, 1991;Pan et al, 2008;Pinto et al, 2007), leukocyte adhesion to the endothelial cells (McLeod et al, 1995;Miyamoto et al, 1996;Schroder et al, 1991), and accumulation of advanced glycation end products (AGEs) 292 (Chibber et al, 1997;Hirata et al, 1997;Kakehashi et al, 2008), are related to the development and progression of diabetic ocular complications. In particular, the polyol pathway is correlated strongly with oxidative stress, activation of PKC, and accumulation of AGEs that lead to induction of vascular endothelial growth factor (VEGF).…”