Advanced glycation endproducts AGEs

Several markers for the Maillard reaction have been described in the literature. For example, the product initially formed between glucose and lysine is partly transformed into furosine (Heyns et ah, 1968) on acid hydrolysis. Conversely, the fluorescent amino acid pentosidine (Sell and Monnier, 1989) is an advanced glycation endproduct (AGE) and may form covalent bonds between proteins (cross-linking). Furthermore, the Maillard reaction leads to an increase in characteristic fluorescence (excitation 370 nm, emission 440 nm) (Monnier et ah, 1984 Pongor et ah, 1984). 

Ahmed, N., Argirov, O.K., Minhas, H.S., Cordeiro, C.A., and Thomalley, P.J. 2002. Assay of advanced glycation endproducts (AGEs) surveying AGEs by chromatographic assay with derivatization by 6-aminoquinolyl-N-hydroxysuccinimidyl-carbamate and application to Nepsilon-carboxymethyl-lysine- and Nepsilon-(l-carboxyethyl)lysine-modified albumin. Biochem J 364 1-14. 

Chronic hyperglycemia induces numerous alterations in the vasculature that accelerate the atherosclerotic process. Several major mechanisms contribute to the pathological alterations in blood vessels in diabetes, including 1) the nonenzymatic glyco-sylation of proteins and lipids, which form advanced glycation endproducts (AGEs) that can interfere with their normal function and 2) the induction of oxidative and nitrosative stress, as well as exacerbation of proinflammatory responses (50). These abnormalities lead to impaired endogenous platelet inhibition and platelet activation, which could result in arterial thrombosis, and consequently myocardial infarction and stroke (51). 

Peyroux J, Sternberg M. Advanced glycation endproducts (AGEs) pharmacological inhibition in diabetes. Pathologie Biologie 2006 54 405 19. 

S. Rahbar and J. L. Figarola, Inhibitors and breakers of advanced glycation endproducts (AGEs) A review, Curr. Med. Chem. Immunol Endocr. Metab. Agents, 2 (2002) 135-161. 

Cai, W., M. Ramdas, L. Zhu et al. Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1. Pmc Natl Acad Sci USA 109(39), 2012 15888-93. 

In Apo E null mice increased Hey by a diet enriched with methionine but depleted in folate, Bg, and B12 increased atherosclerotic lesion area and complexity and enhanced expression of receptor for advanced glycation endproducts (AGE), VCAM-1, TF, and MMP-9 in the vasculature. These effects were suppressed in parallel with decreased plasma Hey levels upon dietary supplementation with folate, Bg, and B12 (7- 5). Also, methionine load increased vWF in patients with arterial or venous occlusive disease with or without hyperhomocysteinemia, suggesting endothelial dysfunction (146). 

Wang R, Kudo M, Yokoyama M, Asano G. Roles of advanced glycation endproducts (AGE) and receptor for AGE on vascular smooth muscle cell growth. J Nippon Med Sch 2001 68 472-481. 

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