Diabetes mellitus is an endocrine metabolic disease of increasing incidence and is associated with serious complications contributing to high morbidity and mortality rates [1]. Several metabolic and signaling pathways become dysfunctional and contribute to chronic disorders associated with diabetes. For example, oxidative stress and advanced glycation end-product (AGE) formation have been identified as key mediators of pathophysiology occurring in diabetes [2].

The combination of oxidative stress and AGEs can elicit irreversible tissue and cellular damage associated with diabetes mellitus and related metabolic disorders [3,4]. The generation of AGEs is a complex process that initially involves a condensation reaction between circulating proteins and glucose, followed by Amadori rearrangement, cyclization, polymerization, cleavage and oxidation processes