Interaction of Some Commercial Teas with Some Carbohydrate Metabolizing Enzymes Linked with Type-2 Diabetes: A Dietary Intervention in the Prevention of Type-2 Diabetes
This study is aimed at assessing the inhibitory effect of teas on key enzymes ( -amylase and -glucosidase) linked with type-2 diabetes and their antioxidant properties. Four samples of three brands were used; infusions of green tea (GT), 2 brands of black tea (BT), and a formulated herbal preparation for diabetes (ADT) (white tea, Radix Puerariae, Radix ophiopogonis, hawthorn berry, Chinese yam, and fragrant Solomon seal rhizome) were prepared and subsequently analyzed for their total phenol, ascorbic acid contents, antioxidant properties (2,2-Azizobis (3-Ethylbenzo-Thiazoline~6-sulfonate) “ABTS” scavenging ability and ferric reducing antioxidant property), and inhibition of pancreatic- -amylase and intestinal- -glucosidase in vitro. The study revealed that GT had the highest total phenol content, ascorbic acid content, ABTS* scavenging ability, and ferric reducing ability. Furthermore, all the teas inhibited Fe2+ and sodium nitroprusside induced lipid peroxidation in pancreas, with GT having the highest inhibitory effect. Conversely, there was no significant difference ( ) in the inhibitory effects of the teas on -amylase and -glucosidase. The antidiabetic property of the teas could be attributed to their inhibitory effect on carbohydrate hydrolyzing enzymes implicated in diabetes and their antioxidant activities. 1. Introduction Diabetes mellitus (DM) is undoubtedly one of the most challenging health problems in the 21st century; statistics show that at 2011, 366 million people are suffering from DM, a figure expected to increase to 552 million people by 2030 [1]. DM is characterized by hyperglycemia associated with abnormal metabolism of carbohydrates, fats, and proteins resulting from endocrine defects in insulin action, secretion, or both [2]. The inhibition of alpha-amylase and alpha-glucosidase, carbohydrate hydrolyzing enzymes, can significantly reduce postprandial hyperglycemia and are thus considered an important therapeutic strategy in the management of blood glucose level in type-2 diabetes [3]. Inhibition of these enzymes delays the breakdown of polysaccharides and glucose absorption, thereby reducing the amount of glucose in the blood [4]. In recent times, there has been a growing interest in medicinal plants and functional foods and their disease modulatory effects. Tea (Camellia sinensis) is the most consumed beverage in the world next to water, its consumption far exceeding beer, wine, and soft drink [5]. Teas are differentiated based on the manufacturing (fermentation) process: green tea (GT)-unfermented and black tea (BT)-fermented
References
[1]
International Diabetes Federation, The Global Burden, 2011, www.idf.org/diabetesatla.
[2]
K. Sama, K. Murugesan, and R. Sivaraj, “In vitro alpha amylase and alpha glucosidase inhibition activity of crude ethanol extract of Cissus arnottiana,” Asian Journal of Plant Science and Research, vol. 2, no. 4, pp. 550–553, 2012.
[3]
R. Tundis, F. Menichini, M. R. Loizzo, M. Bonesi, U. Solimene, and F. Menichini, “Studies on the potential antioxidant properties of Senecio stabianus Lacaita (Asteraceae) and its inhibitory activity against carbohydrate- hydrolysing enzymes,” Natural Product Research, vol. 26, no. 5, pp. 393–404, 2012.
[4]
Y.-I. I. Kwon, D. A. Vattem, and K. Shetty, “Evaluation of clonal herbs of Lamiaceae species for management of diabetes and hypertension,” Asia Pacific Journal of Clinical Nutrition, vol. 15, no. 1, pp. 107–118, 2006.
[5]
Y. Kim, K. L. Goodner, J.-D. Park, J. Choi, and S. T. Talcott, “Changes in antioxidant phytochemicals and volatile composition of Camellia sinensis by oxidation during tea fermentation,” Food Chemistry, vol. 129, no. 4, pp. 1331–1342, 2011.
[6]
C. Anesini, G. E. Ferraro, and R. Filip, “Total polyphenol content and antioxidant capacity of commercially available tea (Camellia sinensis) in Argentina,” Journal of Agricultural and Food Chemistry, vol. 56, no. 19, pp. 9225–9229, 2008.
[7]
P. D. B. Ribaldo, D. S. Souza, S. K. Biswas, K. Block, J. M. L. De Faria, and J. B. L. De Faria, “Green tea (Camellia sinensis) attenuates nephropathy by downregulating Nox4 NADPH oxidase in diabetic spontaneously hypertensive rats,” Journal of Nutrition, vol. 139, no. 1, pp. 96–100, 2009.
[8]
K. A. Grove and J. D. Lambert, “Laboratory, epidemiological, and human intervention studies show that tea (Camellia sinensis) may be useful in the prevention of obesity,” Journal of Nutrition, vol. 140, no. 3, pp. 446–453, 2010.
[9]
M.-H. Yang, C.-H. Wang, and H.-L. Chen, “Green, oolong and black tea extracts modulate lipid metabolism in hyperlipidemia rats fed high-sucrose diet,” The Journal of Nutritional Biochemistry, vol. 12, no. 1, pp. 14–20, 2001.
[10]
S. Archana and J. Abraham, “Comparative analysis of antimicrobial activity of leaf extracts from fresh green tea, commercial green tea and black tea on pathogens,” Journal of Applied Pharmaceutical Science, vol. 1, no. 8, pp. 149–152, 2011.
[11]
T. I. Mbata, L. U. Debiao, and A. Saikia, “Antibacterial activity of the crude extract of Chinese green tea (Camellia sinensis) on Listeria monocytogenes,” African Journal of Biotechnology, vol. 7, no. 10, pp. 1571–1573, 2008.
[12]
G. Oboh and J. B. T. Rocha, “Water extractable phytochemicals from Capsicum pubescens (tree pepper) inhibit lipid peroxidation induced by different pro-oxidant agents in brain: in vitro,” European Food Research and Technology, vol. 226, no. 4, pp. 707–713, 2008.
[13]
K. Hosoda, M.-F. Wang, M.-L. Liao et al., “Antihyperglycemic effect of oolong tea in type 2 diabetes,” Diabetes Care, vol. 26, no. 6, pp. 1714–1718, 2003.
[14]
The InterAct Consortium, “Tea consumption and incidence of type 2 diabetes in Europe: The EPIC-InterAct Case-Cohort Study,” PLOS ONE, vol. 7, no. 5, 2012.
[15]
R. Huxley, C. M. Y. Lee, F. Barzi et al., “Coffee, decaffeinated coffee, and tea consumption in relation to incident type 2 diabetes mellitus: a systematic review with meta-analysis,” Archives of Internal Medicine, vol. 169, no. 22, pp. 2053–2063, 2009.
[16]
M. Benderitter, V. Maupoil, C. Vergely, F. Dalloz, F. Briot, and L. Rochette, “Studies by electron paramagnetic resonance of the importance of iron in the hydroxyl scavenging properties of ascorbic acid in plasma: effects of iron chelators,” Fundamental and Clinical Pharmacology, vol. 12, no. 5, pp. 510–516, 1998.
[17]
V. L. Singleton, R. Orthofer, and R. M. Lamuela-Raventós, “Analysis of total phenols and other oxidation substrates and antioxidants by means of folin-ciocalteu reagent,” Methods in Enzymology, vol. 299, pp. 152–178, 1998.
[18]
R. Re, N. Pellegrini, A. Proteggente, A. Pannala, M. Yang, and C. Rice-Evans, “Antioxidant activity applying an improved ABTS radical cation decolorization assay,” Free Radical Biology and Medicine, vol. 26, no. 9-10, pp. 1231–1237, 1999.
[19]
R. Pulido, L. Bravo, and F. Saura-Calixto, “Antioxidant activity of dietary polyphenols as determined by a modified ferric reducing/antioxidant power assay,” Journal of Agricultural and Food Chemistry, vol. 48, no. 8, pp. 3396–3402, 2000.
[20]
H. Ohkawa, N. Ohishi, and K. Yagi, “Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction,” Analytical Biochemistry, vol. 95, no. 2, pp. 351–358, 1979.
[21]
R. L. Puntel, C. W. Nogueira, and J. B. T. Rocha, “Krebs cycle intermediates modulate thiobarbituric acid reactive species (TBARS) production in rat brain in vitro,” Neurochemical Research, vol. 30, no. 2, pp. 225–235, 2005.
[22]
G. Oboh and T. Henle, “Antioxidant and inhibitory effects of aqueous extracts of Salvia officinalis leaves on pro-oxidant-induced lipid peroxidation in brain and liver in vitro,” Journal of Medicinal Food, vol. 12, no. 1, pp. 77–84, 2009.
[23]
G. Oboh and J. B. T. Rocha, “Antioxidant and neuroprotective properties of sour tea (Hibiscus sabdariffa, calyx) and green tea (Camellia sinensis) on some pro-oxidant-induced lipid peroxidation in brain in vitro,” Food Biophysics, vol. 3, no. 4, pp. 382–389, 2008.
[24]
F. A. Moraes, A. M. Cota, F. M. Campos, and H. M. Pinheiro-Sant'Ana, “Vitamin C loss in vegetables during storage, preparation and distribution in restaurants,” Ciencia e Saude Coletiva, vol. 15, no. 1, pp. 51–62, 2010.
[25]
Y. Y. Lim and E. P. L. Quah, “Antioxidant properties of different cultivars of Portulaca oleracea,” Food Chemistry, vol. 103, no. 3, pp. 734–740, 2007.
[26]
S. J. Padayatty, A. Katz, Y. Wang et al., “Vitamin C as an antioxidant: evaluation of its role in disease prevention,” Journal of the American College of Nutrition, vol. 22, no. 1, pp. 18–35, 2003.
[27]
A. Büyükbalci and S. N. El, “Determination of in vitro antidiabetic effects, antioxidant activities and phenol contents of some herbal teas,” Plant Foods for Human Nutrition, vol. 63, no. 1, pp. 27–33, 2008.
[28]
A. O. Ademosun and G. Oboh, “Inhibition of acetylcholinesterase activity and Fe2+-induced lipid peroxidation in rat brain in vitro by some citrus fruit juices,” Journal of Medicinal Food, vol. 15, no. 5, pp. 428–434, 2012.
[29]
G. Oboh and O. O. Ogunruku, “Cyclophosphamide-induced oxidative stress in brain: protective effect of hot short pepper (Capsicum frutescens L. var. abbreviatum),” Experimental and Toxicologic Pathology, vol. 62, no. 3, pp. 227–233, 2010.
[30]
H. G？？er and I. Gül？in, “Caffeic acid phenethyl ester (CAPE): correlation of structure and antioxidant properties,” International Journal of Food Sciences and Nutrition, vol. 62, no. 8, pp. 821–825, 2011.
[31]
B. C. Adedayo, A. O. Ademiluyi, G. Oboh, and A. A. Akindahunsi, “Interaction of aqueous extracts of two varieties of Yam tubers (Dioscorea spp) on some key enzymes linked to type 2 diabetes in vitro,” International Journal of Food Science and Technology, vol. 47, no. 4, pp. 703–709, 2012.
[32]
P. Carloni, L. Tiano, L. Padella et al., “Antioxidant activity of white, green and black tea obtained from the same tea cultivar,” Food Research International, vol. 53, no. 2, pp. 900–908, 2013.
[33]
E. Niki, Y. Yoshida, Y. Saito, and N. Noguchi, “Lipid peroxidation: mechanisms, inhibition, and biological effects,” Biochemical and Biophysical Research Communications, vol. 338, no. 1, pp. 668–676, 2005.
[34]
Q. A. Nazari, K. Mizuno, T. Kume, Y. Takada-Takatori, Y. Izumi, and A. Akaike, “In vivo brain oxidative stress model induced by microinjection of sodium nitroprusside in mice,” Journal of Pharmacological Sciences, vol. 120, no. 2, pp. 105–111, 2012.
[35]
H.-C. Um, J.-H. Jang, D.-H. Kim, C. Lee, and Y.-J. Surh, “Nitric oxide activates Nrf2 through S-nitrosylation of Keap1 in PC12 cells,” Nitric Oxide, vol. 25, no. 2, pp. 161–168, 2011.
[36]
P. Calcerrada, G. Peluffo, and R. Radi, “Nitric oxide-derived oxidants with a focus on peroxynitrite: molecular targets, cellular responses and therapeutic implications,” Current Pharmaceutical Design, vol. 17, no. 35, pp. 3905–3932, 2011.
[37]
C. Wagner, R. Fachinetto, C. L. D. Corte et al., “Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro,” Brain Research, vol. 1107, no. 1, pp. 192–198, 2006.
[38]
G. Sasipriya and P. Siddhuraju, “Effect of different processing methods on antioxidantactivity of underutilized legumes, Entada scandens seed kernel and Canavalia gladiata seeds,” Food and Chemical Toxicology, vol. 50, no. 8, pp. 2864–2872, 2012.
[39]
G. Oboh and J. B. T. Rocha, “Antioxidant and neuroprotective properties of sour tea (Hibiscus sabdariffa, calyx) and green tea (Camellia sinensis) on some pro-oxidant-induced lipid peroxidation in brain in vitro,” Food Biophysics, vol. 3, no. 4, pp. 382–389, 2008.
[40]
T. Nishikawa, D. Edelstein, X. L. Du et al., “Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage,” Nature, vol. 404, no. 6779, pp. 787–790, 2000.
[41]
O. V. Sakharova, R. R. Lleva, J. D. Dziura et al., “Effects on post-prandial glucose and AGE precursors from two initial insulin strategies in patients with type 2 diabetes uncontrolled by oral agents,” Journal of Diabetes and its Complications, vol. 26, no. 4, pp. 333–338, 2012.
[42]
M. A. Tormo, I. Gil-Exojo, A. Romero de Tejada, and J. E. Campillo, “White bean amylase inhibitor administered orally reduces glycaemia in type 2 diabetic rats,” The British Journal of Nutrition, vol. 96, no. 3, pp. 539–544, 2006.
[43]
M. Yilmazer-Musa, A. M. Griffith, A. J. . Michels, E. Schneider, and B. Frei, “Grape seed and tea extracts and catechin 3-gallates are potent inhibitors of α-Amylase and α-Glucosidase activity,” Journal of Agriculture and Food Chemistry, vol. 60, no. 36, pp. 8924–8929, 2012.
[44]
F. Haidari, M. M. Shahi, M. Zarei, H. Rafiei, and K. Omidian, “Effect of green tea extract on body weight, serum glucose and lipid profile in streptozotocin-induced diabetic rats: a dose response study,” Saudi Medical Journal, vol. 33, no. 2, pp. 128–133, 2012.
