Influence of Tea Polyphenols on the Formation of Advanced Glycation End Products (AGEs) in vitro and in vivo

Shanli Peng¹ and Genyi Zhang^{1, 2,}

¹School of Food Science and Technology, Jiangnan University, Wuxi, China

²State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China

Cite this paper:
Shanli Peng and Genyi Zhang. Influence of Tea Polyphenols on the Formation of Advanced Glycation End Products (AGEs) in vitro and in vivo. Journal of Food and Nutrition Research. 2014; 2(8):524-531. doi: 10.12691/jfnr-2-8-15

Abstract

The effects of tea polyphenols (TP) on the formation of advanced glycation end products (AGEs) were investigated using glutamicacid - glucose and BSA - glucose model systems at 90°C and 37°C, respectively. The spectral characteristics of glycation products were measured. Additionally, a type 1 diabetesmellitus (DM) animal model of Kunming mice by injecting streptozocin (STZ) was used to study the formation of AGEs in vivo. Tea polyphenols (TP) were given to mice at a dose of 200mg/kg bodyweight continuously for 8 weeks. Mice were then sacrificed and the glycosylated hemoglobin (GHbA) and fluorescence of AGEs in serum were measured to illustrate the effects of TP on protein glycation in vivo. The in vitro experiment results showed that the production of AGEs was decreased by TP in a dose-dependent manner TP addition reduced the accumulation of GHbA and AGEs in DM mice and relieved the symptoms of diabetic nephropathy (DN), which is an important indicator of diabetic complications caused by AGEs. Thus, TP might be used as an important ingredient in dietary approaches for intervention of diabetes and improved health.

Keywords:
tea polyphenols advanced glycation end products (AGEs) diabetes mellitus antioxdation

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References:

[1]	Rincon, N., et al., Update of Retraction--Blockade of Receptor for Advanced Glycation End Products in a Model of Type 1 Diabetic Leukoencephalopathy. Diabetes. 19 November 2012 Epub ahead of print. Diabetes, 2014. 63(5): 1817-1817.
[2]	Turk, Z., S. Ljubic, and J. Boras, Decreased level of endogenous secretory receptor for advanced glycation end-products in diabetes with concomitant hyperlipidemia. Physiological research / Academia Scientiarum Bohemoslovaca, 2014. 63(2): 199-205.
[3]	Lovestone, S. and U. Smith, Advanced glycation end products, dementia, and diabetes. Proceedings of the National Academy of Sciences of the United States of America, 2014. 111(13): 4743-4744.
[4]	Barzilay, J.I., et al., The Impact of Salsalate Treatment on Serum Levels of Advanced Glycation End Products in Type 2 Diabetes. Diabetes Care, 2014. 37(4): 1083-1091.
[5]	Yamagishi, S. and T. Matsui, Advanced Glycation End Products (AGEs), Oxidative Stress and Diabetic Retinopathy. Current Pharmaceutical Biotechnology, 2011. 12(3): 362-368.
[6]	Daroux, M., et al., Advanced glycation end-products: implications for diabetic and non-diabetic nephropathies. Diabetes Metab, 2010. 36(1): 1-10.
[7]	Singh, R., et al., Advanced glycation end-products: a review. Diabetologia, 2001. 44(2): 129-46.
[8]	Vlassara, H. and G.E. Striker, AGE restriction in diabetes mellitus: a paradigm shift. Nature Reviews Endocrinology, 2011. 7(9): 526-539.
[9]	Montonen, J., et al., Dietary antioxidant intake and risk of type 2 diabetes. Diabetes Care, 2004. 27(2): 362-6.
[10]	Das, D., et al., Aqueous extract of black tea (Camellia sinensis) prevents chronic ethanol toxicity. Current Science, 2005. 88(6): 952-961.
[11]	El-Masry, E.M. and M.B. Abou-Donia, Reversal of P-glycoprotein expressed in Escherichia coli leaky mutant by ascorbic acid. Life Sciences, 2003. 73(8): 981-91.
[12]	Jeukendrup, A.E., et al., Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. American Journal of Clinical Nutrition, 2008. 87(3): 778-784.
[13]	Venables, M.C., et al., Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. American Journal of Clinical Nutrition, 2008. 87(3): 778-784.
[14]	Hossain, M.A. and S.M.M. Rahman, Total phenolics, flavonoids and antioxidant activity of tropical fruit pineapple. Food Research International, 2011. 44(3): 672-676.
[15]	Ramadan, G., N.M. El-Beih, and E.A.A. El-Ghffar, Modulatory effects of black v. green tea aqueous extract on hyperglycaemia, hyperlipidaemia and liver dysfunction in diabetic and obese rat models. British Journal of Nutrition, 2009. 102(11): 1611-1619.
[16]	Kai Zhong1, et al., Antioxidant and Cytoprotective Activities of Flavonoid Glycosides-rich Extract from the Leaves of Zanthoxylum bungeanum. Journal of Food and Nutrition Research, 2014. 2(7): 349-356.
[17]	DIMITRIJEVIĆ, D.S., et al., Phenolic composition, antioxidant activity, mineral content and antimicrobial activity of fresh fruit extracts of Morus alba L. Journal of Food and Nutrition Research, 2014(1): 22-30.
[18]	Farrar, J.L., et al., A novel nutraceutical property of select sorghum (Sorghum bicolor) brans: inhibition of protein glycation. Phytotherapy Research, 2008. 22(8): 1052-6.
[19]	Wang, J., et al., Protein glycation inhibitory activity of wheat bran feruloyl oligosaccharides. Food Chemistry, 2009. 112(2): 350-353.
[20]	Yokozawa, T. and T. Nakagawa, Inhibitory effects of Luobuma tea and its components against glucose-mediated protein damage. Food and Chemical Toxicology, 2004. 42(6): 975-81.
[21]	Yin, J., et al., Epicatechin and epigallocatechin gallate inhibit formation of intermediary radicals during heating of lysine and glucose. Food Chemistry, 2014. 146: 48-55.
[22]	Ajandouz, E., et al., Effects of pH on Caramelization and Maillard Reaction Kinetics in Fructose‐Lysine Model Systems. Journal of Food Science, 2001. 66(7): 926-931.
[23]	Guneli, E., et al., Effect of melatonin on testicular damage in streptozotocin-induced diabetes rats. Eur Surg Res, 2008. 40(4): 354-60.
[24]	Çağlarırmak, N., Biochemical properties of tea constituents. 2nd ConferenceFoods and Nutraceaticals.2006. P: 59. İstanbul, 4-6 mayıs.P. 59.
[25]	Obayashi, H., et al., Formation of crossline as a fluorescent advanced glycation end product in vitro and in vivo. Biochemical and Biophysical Research Communications, 1996. 226(1): 37-41.
[26]	Leclere, J. and I. Birlouez-Aragon, The fluorescence of advanced Maillard products is a good indicator of lysine damage during the Maillard reaction. Journal of Agricultural and Food Chemistry, 2001. 49(10): 4682-4687.
[27]	Rondeau, P., et al., Thermal aggregation of glycated bovine serum albumin. Biochimica Et Biophysica Acta-Proteins and Proteomics, 2010. 1804(4): 789-798.
[28]	Reed, M.J., et al., A new rat model of type 2 diabetes: the fat-fed, streptozotocin-treated rat. Metabolism, 2000. 49(11): 1390-4.
[29]	Manley, S.E., et al., Validation of an algorithm combining haemoglobin A(1c) and fasting plasma glucose for diagnosis of diabetes mellitus in UK and Australian populations. Diabetic Medicine, 2009. 26(2): 115-121.
[30]	Lindsey, J.B., et al., Receptor for advanced glycation end-products (RAGE) and soluble RAGE (sRAGE): cardiovascular implications. Diab Vasc Dis Res, 2009. 6(1): 7-14.
[31]	Wendt, T., et al., Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy. J Am Soc Nephrol, 2003. 14(5): 1383-95.
[32]	Wendt, T.M., et al., RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. American Journal of Pathology, 2003. 162(4): 1123-1137.
[33]	Pan, H.Z., et al., The oxidative stress status in diabetes mellitus and diabetic nephropathy. Acta Diabetologica, 2010. 47: S71-S76.
[34]	Harja, E., et al., Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/-mice. Journal of Clinical Investigation, 2008. 118(1): 183-194.
[35]	Miyata, T., et al., Implication of an increased oxidative stress in the formation of advanced glycation end products in patients with end-stage renal failure. Kidney International, 1997. 51(4): 1170-1181.
[36]	Rahbar, S. and J.L. Figarola, Novel inhibitors of advanced glycation endproducts. Archives of Biochemistry and Biophysics, 2003. 419(1): 63-79.
[37]	Scalbert., A. and G. Williamson., Dietary Intake and Bioavailability of Polyphenols. J. Nutr., 2000. 130: 2073-2085.
[38]	Peters, C.M., et al., ！Formulation with ascorbic acid and sucrose modulates catechin bioavailability from green tea. Food Research International, 2010. 43(1): 95-102.
[39]	Scalbert, A., et al., Absorption and metabolism of polyphenols in the gut and impact on health. Biomedecine & Pharmacotherapy, 2002. 56(6): 276-282.
[40]	Donovan, J.L., et al., Catechin is metabolized by both the small intestine and liver of rats. The Journal of nutrition, 2001. 131(6): 1753.