Previous research has demonstrated that chronic hyperglycemia plays a leading role in the development of vascular dysfunction and damage in individuals with T2DM, primarily involving the aldose reductase, polyol pathway (Greene et al., 1987; Kador et al., 1985), alteration of oxidation reduction potential (Tilton et al., 1992; Williamson et al., 1993), diacylglycerol‐protein kinase C pathway (Kikkawa & Nishizuka, 1986), and the accumulation of advanced glycosylation end products. This evidence concerns the gene AKR1B1 and type 2 diabetes mellitus.