European Journal of Molecular & Clinical Medicine

Abstract

Diabetic complications, such as, retinopathy, nephropathy lead to blindness and end stage renal failure respectively, various neuropathies, and ultimately increased mortality. While the exact mechanisms that lie behind the pathological changes associated with diabetes remain obscure, however, it is widely believed that chronic or intermittent hyperglycemia may alter various metabolic pathways at the tissue level, for instance, increased flux through the polyol and the hexosamine pathways as well as a persistent activation of protein kinase C (PKC). Reducing sugars such as glucose and fructose may react non-enzymatically through their carbonyl groups with free amino groups of proteins (commonly the Ɛ amino group of lysine) to form a Schiff base intermediate which then rearranges to a more stable structure known as Amadori product. The Amadori products generated by the aforementioned Maillard reaction may then undergo further reactions, including dehydration, oxidation and rearrangement resulting in the irreversible formation of heterogeneous advanced glycation end products (AGEs)