Endogenous Glycation and its Effect on Human Health

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Endogenous glycation is the chemical result of the bonding of a sugar molecule with a protein or lipid molecule that produces nonfunctioning and deformed molecules known as advanced glycation end products (AGE’s).

AGE’s that stem from a glycation reaction, produces cells that are stiffer and less pliable and more subject to damage and premature aging. When glycated proteins fuse together, this is known as cross-linking. The skin, eyes and heart are particular organs subject to cross-linking.

Exogenous glycation occurs when AGE’s are formed by heating proteins and lipids with sugar. Certain forms of cooking can accelerate the exogenous glycation process, such as grilling and frying.

AGEs have a range of pathological effects, such as:

  • Increased vascular permeability.
  • Oxidizing LDL.
  • Binding cells—including macrophage, endothelial, and mesangial—to induce the secretion of a variety of cytokines – promoting chronic inflammation.
  • Inhibition of vascular dilation by interfering with nitric oxide.
  • Enhanced oxidative stress – free radicals.

Once an AGE is produced through the endogenous glycation process, it is irreversible. It is therefore important to seek ways to prevent glycation, both endogenously and exogenously.

Compounds that are thought to inhibit AGE formation, at least in vitro, include:

Vitamins

  • Vitamin C [1]
  • Vitamin E [2]
  • Nicotinic Acid [3]
  • Benfotiamine [4]
  • Pyridoxamine [5]
  • Alpha-lipoic acid [6]
  • Pyridoral-5-phosphate (P-5-P) [7]

Amino Acids

  • Taurine [8]
  • Carnosine [9]
  • Beta-Alanine
  • Acety-L-Carnitine [10]
  • Ethylene-Diamine-Tetra-Acetate (EDTA) [11]

Minerals

  • Chromium [12]
  • Zinc [13]

Polyphenols

  • Diosmin [14]
  • Oligomeric Proanthocyanidins [15]
  • Quercetin [16]
  • Rutin [17]

Nootropics

  • Centrophenoxine [18]
  • Dimethylaminoethanol (DMAE) [19]

Herbs

  • Rosemary [20]
  • Astagalus [21]

Pharmaceuticals (Prescription required by licensed physician):

  • Acarbose [22]
  • Metformin [23]
  • Aminoguanidine [24]

Compounds that are thought to break some existing AGE crosslinks include:

  • Alagebrium (and related compounds ALT-462; ALT-486; ALT-946) [25]
  • N-phenacyl thiazolium bromide

References:

[1] Krone, C. A., et al. Ascorbic acid, glycation, glycohemoglobin and aging. Med Hypotheses. 62(2):275-279, 2004.

[2] Alderson, N. L., et al. Effect of antioxidants and ACE inhibition on chemical modification of proteins and progression of nephropathy in the streptozotocin diabetic rat. Diabetologia. 47(8):1385-1395, 2004.

[3] Rahbar, S., et al. Niacin (3-Pyridinecarboxylic Acid) is a potent inhibitor of advanced glycation endproducts (AGE’s). Diabetes. 48(5):SA375, 1999.

[4] Stirban, A., et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care. 29:2064-2071, 2006.

[5] Jain, S. K., et al. Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes. Free Radic Biol Med. 30(3):232-237, 2001.

[6] Jain, S. K., et al. Lipoic acid decreases lipid peroxidation and protein glycosylation and increases (Na(+) + K(+))- and Ca(++)-ATPase activities in high glucose-treated human erythrocytes. Free Radic Biol Med. 29:1122-1128, 2000.

[7] Higuchi, O., et al. Aminophospholipid glycation and its inhibitor screening system: A new role of pyridoxal 5′-phosphate and pyridoxal as lipid glycation inhibitor. Journal of Lipid Research. 2006.

[8] Nandhini, A. T., et al. Stimulation of glucose utilization and inhibition of protein glycation and AGE products by taurine. Acta Physiol Scand. 181(3):297-303, 2004.

[9] Brownson, C., et al. Carnosine reacts with a glycated protein. Free Radic Biol Med. 28(10):1564-1570, 2000.

[10] Swamy-mruthinti, S., et al. Acetyl-L-carnitine decreases glycation of lens proteins: in vitro studies. Exp Eye Res. 69(1):109-115, 1999.

[11] Jorksten, J. Pathways to the decisive extension of the human specific lifespan. J American Geriatrics Society. 25:396-399, 1977.

[12] Evans, G. W. Conference of the American Aging Association. San Franciscio, California, USA. October 1992.

[13] Tupe, R., et al. Interaction of zinc, ascorbic acid, and folic acid in glycation with albumin as protein model. Biol Trace Elem Res. 2010.

[14] Manuel, Y., et al. The effect of flavonoid treatment on the glycation antioxidant status in Type-1 diabetic patients. Diabetes Nutr Metab. 12(4):256-263, 1999.

[15] Urios, P., et al. Flavonoids inhibit the formation of the cross-linking AGE pentosidine in collagen incubated with glucose, according to their structure. European Journal of Clinical Nutrition. 2007.

[16] Urios, P., et al. Flavonoids inhibit the formation of the cross-linking AGE pentosidine in collagen incubated with glucose, according to their structure. European Journal of Clinical Nutrition. 2007.

[17] Cervantes-Laurean, D., et al. Inhibition of advanced glycation end product formation on collagen by rutin and its metabolites. Journal of Nutritional Biochemistry. 2005.

[18] Nagy, I., et al. On the role of cross-linking of cellular proteins in aging. Mech Aging Dev. 14(1-2):245-251, 1980.

[19] Nagy, I., et al. On the role of cross-linking of cellular proteins in aging. Mech Aging Dev. 14(1-2):245-251, 1980.

[20] Dearlove, R. P., et al. Inhibition of protein glycation by extracts of culinary herbs and spices. Journal of Medicinal Food. 11(2):275-281, 2008.

[21] Motomura, K., et al. Astragalosides isolated from the root of Astragalus Radix inhibit the formation of advanced glycation end products. J Agric Food Chem. 2009.

[22] Cohen, M. P., et al. Alpha-glucosidase inhibition prevents increased collagen fluorescence in experimental diabetes. Gen Pharmacol. 22(4):607-610, 1991.

[23] Beisswenger, P., et al. Metformin inhibition of glycation processes. Diabetes Metab. 29(4 Part 2):95-103, 2003.

[24] Corman, B., et al. Aminoguanidine prevents age-related arterial stiffening and cardiac hypertrophy. Proceedings of the National Academy of Sciences of the United States of America. 95(3):1301-1306, 1998.

[25] Asif, M., et al. An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness. Proc Natl Acad Sci USA. 97(6):2809-2813, 2000.


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