Additional benefit of higher dose green tea in lowering postprandial blood glucose

  • Rita Lahirin Department of Nutrition, Faculty of Medicine Universitas Indonesia, Jakarta
  • Inge Permadhi Department of Nutrition, Faculty of Medicine Universitas Indonesia, Jakarta
  • Ninik Mudjihatini Department of Biochemistry, Faculty of Medicine Universitas Indonesia, Jakarta
  • Rahmawaty Ridwan Department of Biochemistry, Faculty of Medicine Universitas Indonesia, Jakarta
  • Ray Sugianto Department of Nutrition, Faculty of Medicine Universitas Indonesia, Jakarta
Keywords: cathecin, green tea, postprandial blood glucose
Abstract viewed: 2697 times
PDF downloaded: 1003 times

Abstract

Background: Green tea contains catechins that have inhibitory effects on amylase, sucrase, and sodium-dependent glucose transporter (SGLT) which result in lowering of postprandial blood glucose (PBG). This beneficial effect has been widely demonstrated using the usual dose (UD) of green tea preparation. Our study was aimed to explore futher lowering of PBG using high dose (HD) of green tea in healthy adolescents.

Methods: 24 subjects received 100 mL infusion of either 0.67 or 3.33 grams of green tea with test meal. Fasting, PBG at 30, 60, 120 minutes were measured. Subjects were cross-overed after wash out. PBG and its incremental area under the curve (IAUC) difference between groups were analyzed with paired T-test. Cathecin contents of tea were measured using high-performance liquid chromatography (HPLC).

Results: The PBG of HD group was lower compared to UD (at 60 minutes =113.70 ± 13.20 vs 124.16 ± 8.17 mg/dL, p = 0.005; at 120 minutes = 88.95 ± 6.13 vs 105.25 ± 13.85 mg/dL, p < 0.001). The IAUC of HD was also found to be lower compared to UD (2055.0 vs 3411.9 min.mg/dL, p < 0.001).

Conclusion: Additional benefit of lowering PBG can be achieved by using higher dose of green tea. This study recommends preparing higher dose of green tea drinks for better control of PBG.

Downloads

Download data is not yet available.

References

  1. Perkumpulan Endokrinologi Indonesia. Konsensus Pengendalian dan Pencegahan Diabetes Mellitus Tipe2 di Indonesia Jakarta: PB PERKENI; 2011. Indonesian.

  2. Alan JG. American College of Endocrinology and American Diabetes Association Consensus statement on inpatient diabetes and glycemic control. Diabetes Care. 2006;29(8):1955-62. http://dx.doi.org/10.2337/dc06-9913

  3. Grooper SS, Smith JL, Groff JL. Advance nutrition and human metabolism. 5th ed. USA: Wadsworth Cengage Learning. 2009. p. 63-123.

  4. Direktorat Pengendalian Penyakit Tidak Menular dan Penyehatan Lingkungan, Departemen Kesehatan RI. Pedoman teknis penemuan dan tatalaksana penyakit diabetes melitus. Jakarta; 2008.

  5. Del Rio D, Borges G, Crozier A. Berry flavonoids and phenolics: bioavailability and evidence of protective effects. Br J Nutr. 2010;104(Suppl3):S67-90. doi: 10.1017/S0007114510003958.

  6. Namita P, Mukesh R, Vijay KJ. Camellia sinensis (green tea): a review. Global J Pharmacol. 2012;6(2):52-9.

  7. Bhatt PR, Pandya KB, Sheth NR. Camellia sinensis (L): the medical beverage. Int J Pharmaceut Sci. 2010;3(2):6-9.

  8. Babu PV, Liu D. Green tea catechins and cardiovascular health: an update. Curr Med Chem. 2008;15(18):1840-50. http://dx.doi.org/10.2174/092986708785132979

  9. Bahoran T, Soobrattee MA, Ramma-Luximon V, OI Aruoma. Free radicals and antioxidants in cardiovascular health and disease. Internet J of Med Update. 2006;1(2):25-41. http://dx.doi.org/10.4314/ijmu.v1i2.39839

  10. Cabrera C, Artacho R, Giménez R. Beneficial effects of green tea - a review. J Am Coll Nutr. 2006;25(2):79-99. http://dx.doi.org/10.1080/07315724.2006.10719518

  11. Kobayashi Y, Suzuki M, Satsu H, Arai S, Hara Y, Suzuki K, et al. Green tea polyphenols inhibit the sodium-dependent glucose transporter of intestinal epithelial cells by a competitive mechanism. J Agric Food Chem. 2000;48(11):5618-23. http://dx.doi.org/10.1021/jf0006832

  12. Stote KS, Bae DJ. Tea consumption may improve biomarkers of insulin sensitivity and risk factors for diabetes. J Nutr. 2008;138(1):1584S-8S.

  13. Lee YJ, Jeong KW, Kim Y. Epigallocatechin 3-gallate binds to human salivary α-amylase with complex hydrogen bonding interactions. Bull Korean Chem Soc. 2011;32(7):2222-6. http://dx.doi.org/10.5012/bkcs.2011.32.7.2222

  14. Durak ZE, Öztürk B. Effects of black and green tea extracts on glucose utilisation rate in bovine skeletal muscle in vitro. Int Inv J Biochem Bioinform. 2013;1(1):5-8.

  15. Nagao T, Meguro S, Hase T, Otsuka K, Komikado M, Tokimutsu I, et al. A catechin-rich beverage improves obesity and blood glucose control in patients with type 2 diabetes. Obesity (Silver Spring). 2008;17(2):310-7. http://dx.doi.org/10.1038/oby.2008.505

  16. Tsuneki H, Ishizuka M, Terasawa M, Wu JB, Sasaoka T, Kimura I. Effect of green tea on blood glucose levels and serum proteomic patterns in diabetic (db/db) mice and on glucose metabolism in healthy humans. BMC Pharmacol. 2004;4(18):1-10. doi: 10.1186/1471-2210-4-18

  17. Josic J, Olsson AT, Wickeberg J, Lindstedt S, Hlebowicz J. Does green tea affect postprandial glucose, insulin and satiety in healthy subjects: a randomized controlled trial. J Nutr. 2010;9(63):1-8. http://dx.doi.org/10.1186/1475-2891-9-63

  18. Ryu OH, Lee J, Lee KW, Kim HY, Seo JA, Kim SG, et al. Effects of green tea consumption on inflammation, insulin resistance and pulse wave velocity in type 2 diabetes patients. Diabetes Res Clin Pract. 2006;71(3):356-8. http://dx.doi.org/10.1016/j.diabres.2005.08.001

  19. Babu VP, Liu D. Green tea catechins and cardiovascular health: an update. Curr Med Chem. 2008;15(18):1840-50. http://dx.doi.org/10.2174/092986708785132979

  20. Thielecke F, Boschmann M. The potential role of green tea catechins in the prevention of the metabolic syndrome - a review. Phytochemistry. 2009;70(1):11-24. http://dx.doi.org/10.1016/j.phytochem.2008.11.011

  21. World Health Organization. The Asia-Pacific perspective: Redefining obesity and its treatment. Australia: Health Communication; 2000. p.18.

  22. Hendarwanto, Waspadji S, Markum HMS. Pemeriksaan fisis umum. In: Markum HMS. Penuntun anamnesis dan pemeriksaan fisis. Jakarta: Pusat Penerbitan Departemen Ilmu Penyakit Dalam Fakultas Kedokteran Universitas Indonesia; 2005. p. 54-5. Indonesian.

  23. Garber AJ, Abrahamson MJ, Barzilay JI, Blonde L, Bloomgarden ZT, et al. American Association of Clinical Endocrinogists' comprehensive diabetes management algorithm 2013 consensus statement. Endocr Pract. 2013;19(Suppl2):1-48. DOI:10.4158/EP13176.CSUPPL

  24. Wolever TM, Ming Y, Zeng XY, Atkinson F, Brand-Miller JC. Food glycemic index, as given in glycemic index tables, is a significant determinant of glycemic responses elicited by composite breakfast meals. Am J Clin Nutr. 2006;83(6):1306-12.

  25. Iso H, Date C, Wakai K, Fukui M, Tamakoshi A, JAC Study Group. The relationship between green tea and total caffeine intake and risk for self-reported type 2 diabetes among Japanese adults. Ann Intern Med. 2006;144(8):554-62. http://dx.doi.org/10.7326/0003-4819-144-8-200604180-00005

  26. Jing Y, Han G, Hu Y, Bi Y, Li L, Zhu D. Tea consumption and risk of type 2 diabetes: a meta-analysis of cohort studies. J Gen Intern Med. 2009;24(5):557-62. http://dx.doi.org/10.1007/s11606-009-0929-5

  27. Rodwin AJ. Mechanism of age related-glucose tolerance. Diabetes Care. 1990;13(Suppl2):9-19. doi: 10.2337/diacare.13.2.S9

  28. Basu R, Dalla Man C, Campioni M, Basu A, Klee G, Toffolo G, et al. Effects of age and sex on postprandial glucose metabolism: differences in glucose turnover, insulin secretion, insulin action, and hepatic insulin extraction. Diabetes. 2006;55(7):2001-14. http://dx.doi.org/10.2337/db05-1692

  29. Mark DB, Mark AD, Smith CM. Carbohydrate Metabolism. Basic medical biochemistry: A clinical approach USA: Lippincott Williams & Wilkins; 2011. p. 493-580.

  30. Guyton AC, Hall JE. Textbook of medical physiology. Insulin, glucagon, and diabetes melitus. 11th ed. Philadelphia: Elsevier; 2006. p. 961-77.

  31. Sherwood L. Human physiology from cells to systems. The digestive system. 7th ed. USA: Brooks/Cole Cengage Learning; 2010. p. 589-639.

  32. Hara Y, Honda M. The inhibition of a-amylase by tea polyphenols. Agricul Biol Chem 1990;54(8):1939-45. http://dx.doi.org/10.1271/bbb1961.54.1939

  33. Forester SC, Gu Y, Lambert JD. Inhibition of starch digestion by the green tea polyphenol, (-)-epigallocatechin-3- gallate. Mol Nutr Food Res. 2012;56(11):1647-54. http://dx.doi.org/10.1002/mnfr.201200206

  34. Snoussi C, Ducroc R, Hamdaoui MH, Dhaouadi K, Abaidi H, Cluzeaud F, et al. Green tea decoction improves glucose tolerance and reduces weight gain of rats fed normal and high-fat diet. J Nutr Biochem. 2014;25(5):557-64. http://dx.doi.org/10.1016/j.jnutbio.2014.01.006

  35. Yashin A, Nemzer B, Yashin Y. Bioavailability of tea components. J Food Res. 2012;1(1):281-90. http://dx.doi.org/10.5539/jfr.v1n2p281

  36. Babu PV, Sabitha KE, Shyamaladevi CS. Therapeutic effect of green tea extract on oxidative stress in aorta and heart of streptozotocin diabetic rats. Chem Biol Interact. 2006;162(2):114-20. http://dx.doi.org/10.1016/j.cbi.2006.04.009

  37. Sheperd PR, Kahn BB. Glucose transporters and insulin action--implications for insulin resistance and diabetes mellitus. N Engl J Med. 1999;341(4):248-57. http://dx.doi.org/10.1056/NEJM199907223410406

  38. Hara Y. Green tea: health benefits and application. New York: Basel; 2011. p.11-47.

Published
2015-06-17
How to Cite
1.
Lahirin R, Permadhi I, Mudjihatini N, Ridwan R, Sugianto R. Additional benefit of higher dose green tea in lowering postprandial blood glucose. Med J Indones [Internet]. 2015Jun.17 [cited 2024Oct.7];24(2):97-102. Available from: https://mji.ui.ac.id/journal/index.php/mji/article/view/1167
Section
Clinical Research