The biochemical process of advanced glycation appears to play a central role in the development and progression of diabetic vascular complications.
Association studies have been carried out with DN candidate genes that regulate blood pressure, the synthesis and degradation of renal structural components, the metabolism and transport of glucose and the process of advanced glycation [ 1, 13, 14].
A recent study on bovine cartilage indicated that the release of high mobility group box chromosomal protein 1 (HMGB-1) and receptor for advanced glycation end product (RAGE -mediated pRAGE -mediatedy exprocessese chemotactic effect [ 26].
Endogenous compounds in SSBs, such as advanced glycation end products, produced during the process of caramelization in cola-type beverages may also affect pathophysiological pathways related to type 2 diabetes and metabolic syndrome (31).
During the ageing process, there is a phenomenon characterized by post-translational modification of proteins by non-enzymatic glycation and this process results in accumulation of advanced glycation end products (AGEs) in many tissues, including joints [ 3, 4].
Ageing involves systemic accumulation of advanced glycation end products (AGEs), a diverse class of compounds resulting from glycation process under the strong influence of oxidative or carbonyl stress (Schleicher et al. 1997).
It has become apparent that advanced glycation end products (AGEs) can regulate many cardiovascular disease processes through changes in endothelial cell and platelet function.
In addition, other processes related to diabetes, such as advanced glycation end product accumulation or changes in cerebral insulin signaling, may promote Alzheimer's disease (7).
It has been demonstrated that advanced glycation end-products (AGEs) may be involved in different processes associated with urticarial inflammation, including complement activation, release of inflammatory cytokines, increase of vascular permeability, and procoagulant effects [ 10– 10].
Enhanced formation and accumulation of advanced glycation endproducts (AGEs), have been implicated as a major pathogenesis process leading to diabetic complications, normal aging, atherosclerosis, and Alzheimer's Disease.
Furthermore, this induction was neutralized by an anti-receptor for advanced glycation end products (RAGE) antibody, indicating RAGE engagement in this process.
