期刊论文详细信息
Nutrition & Metabolism
Diet supplementation with green tea extract epigallocatechin gallate prevents progression to glucose intolerance in db/db mice
Åke Sjöholm3  Nicolas Kuehn2  Swen Wolfram1  Nina Grankvist3  Henrik Ortsäter3 
[1] DSM Nutritional Products Ltd, Department of Human Nutrition and Health, P.O. Box 2676, Bldg.241/958, CH-4002 Basel, Switzerland;Diavet Labor, Schlyffistrasse 10, CH-8806, Bäch/SZ Zurich, Switzerland;Karolinska Institutet, Department of Clinical Science and Education, Södersjukhuset, SE-118 83 Stockholm, Sweden
关键词: Insulin secretion;    Beta cell;    Diabetes islet;    Epigallocatechin gallate;    Green tea;   
Others  :  820087
DOI  :  10.1186/1743-7075-9-11
 received in 2012-01-03, accepted in 2012-02-14,  发布年份 2012
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【 摘 要 】

Background

Green tea was suggested as a therapeutic agent for the treatment of diabetes more than 70 years ago, but the mechanisms behind its antidiabetic effect remains elusive. In this work, we address this issue by feeding a green tea extract (TEAVIGO™) with a high content of epigallocatechin gallate (EGCG) or the thiazolidinedione PPAR-γ agonist rosiglitazone, as positive control, to db/db mice, an animal model for diabetes.

Methods

Young (7 week-old) db/db mice were randomized and assigned to receive diets supplemented with or without EGCG or rosiglitazone for 10 weeks. Fasting blood glucose, body weight and food intake was measured along the treatment. Glucose and insulin levels were determined during an oral glucose tolerance test after 10 weeks of treatment. Pancreata were sampled at the end of the study for blinded histomorphometric analysis. Islets were isolated and their mRNA expression analyzed by quantitative RT-PCR.

Results

The results show that, in db/db mice, EGCG improves glucose tolerance and increases glucose-stimulated insulin secretion. EGCG supplementation reduces the number of pathologically changed islets of Langerhans, increases the number and the size of islets, and heightens pancreatic endocrine area. These effects occurred in parallel with a reduction in islet endoplasmic reticulum stress markers, possibly linked to the antioxidative capacity of EGCG.

Conclusions

This study shows that the green tea extract EGCG markedly preserves islet structure and enhances glucose tolerance in genetically diabetic mice. Dietary supplementation with EGCG could potentially contribute to nutritional strategies for the prevention and treatment of type 2 diabetes.

【 授权许可】

   
2012 Ortsater et al; licensee BioMed Central Ltd.

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【 参考文献 】
  • [1]Yang CS, Wang ZY: Tea and cancer. J Natl Cancer Inst 1993, 85:1038-1049.
  • [2]Anderson RA, Polansky MM: Tea enhances insulin activity. J Agric Food Chem 2002, 50:7182-7186.
  • [3]Hamilton-Miller JM: Antimicrobial properties of tea (Camellia sinensis L.). Antimicrob Agents Chemother 1995, 39:2375-2377.
  • [4]Katiyar SK, Mukhtar H: Tea consumption and cancer. World Rev Nutr Diet 1996, 79:154-184.
  • [5]Maron DJ, Lu GP, Cai NS, Wu ZG, Li YH, Chen H, Zhu JQ, Jin XJ, Wouters BC, Zhao J: Cholesterol-lowering effect of a theaflavin-enriched green tea extract: a randomized controlled trial. Arch Intern Med 2003, 163:1448-1453.
  • [6]Waltner-Law ME, Wang XL, Law BK, Hall RK, Nawano M, Granner DK: Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem 2002, 277:34933-34940.
  • [7]Han MK: Epigallocatechin gallate, a constituent of green tea, suppresses cytokine-induced pancreatic beta-cell damage. Exp Mol Med 2003, 35:136-139.
  • [8]Song EK, Hur H, Han MK: Epigallocatechin gallate prevents autoimmune diabetes induced by multiple low doses of streptozotocin in mice. Arch Pharm Res 2003, 26:559-563.
  • [9]Abe I, Kashiwagi K, Noguchi H: Antioxidative galloyl esters as enzyme inhibitors of p-hydroxybenzoate hydroxylase. FEBS Lett 2000, 483:131-134.
  • [10]Suh KS, Chon S, Oh S, Kim SW, Kim JW, Kim YS, Woo JT: Prooxidative effects of green tea polyphenol (-)-epigallocatechin-3-gallate on the HIT-T15 pancreatic beta cell line. Cell Biol Toxicol 2009, 26:189-199.
  • [11]Reeves PG: Components of the AIN-93 diets as improvements in the AIN-76A diet. J Nutr 1997, 127:838S-841S.
  • [12]Livak KJ, Schmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods 2001, 25:402-408.
  • [13]Weir GC, Bonner-Weir S: Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes 2004, 53(Suppl 3):S16-S21.
  • [14]Laybutt DR, Preston AM, Akerfeldt MC, Kench JG, Busch AK, Biankin AV, Biden TJ: Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes. Diabetologia 2007, 50:752-763.
  • [15]Song B, Scheuner D, Ron D, Pennathur S, Kaufman RJ: Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes. J Clin Invest 2008, 118:3378-3389.
  • [16]Buckingham RE, Al-Barazanji KA, Toseland CD, Slaughter M, Connor SC, West A, Bond B, Turner NC, Clapham JC: Peroxisome proliferator-activated receptor-gamma agonist, rosiglitazone, protects against nephropathy and pancreatic islet abnormalities in Zucker fatty rats. Diabetes 1998, 47:1326-1334.
  • [17]Assimacopoulos-Jeannet F, Thumelin S, Roche E, Esser V, McGarry JD, Prentki M: Fatty acids rapidly induce the carnitine palmitoyltransferase I gene in the pancreatic beta-cell line INS-1. J Biol Chem 1997, 272:1659-1664.
  • [18]Wolfram S, Raederstorff D, Preller M, Wang Y, Teixeira SR, Riegger C, Weber P: Epigallocatechin gallate supplementation alleviates diabetes in rodents. J Nutr 2006, 136:2512-2518.
  • [19]Rubi B, Antinozzi PA, Herrero L, Ishihara H, Asins G, Serra D, Wollheim CB, Maechler P, Hegardt FG: Adenovirus-mediated overexpression of liver carnitine palmitoyltransferase I in INS1E cells: effects on cell metabolism and insulin secretion. Biochem J 2002, 364:219-226.
  • [20]Ozcan U, Cao Q, Yilmaz E, Lee AH, Iwakoshi NN, Ozdelen E, Tuncman G, Gorgun C, Glimcher LH, Hotamisligil GS: Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science 2004, 306:457-461.
  • [21]Marchetti P, Bugliani M, Lupi R, Marselli L, Masini M, Boggi U, Filipponi F, Weir GC, Eizirik DL, Cnop M: The endoplasmic reticulum in pancreatic beta cells of type 2 diabetes patients. Diabetologia 2007, 50:2486-2494.
  • [22]Bone AJ, Hii CS, Brown D, Smith W, Howell SL: Assessment of the antidiabetic activity of epicatechin in streptozotocin-diabetic and spontaneously diabetic BB/E rats. Biosci Rep 1985, 5:215-221.
  • [23]Chakravarthy BK, Gupta S, Gambhir SS, Gode KD: Pancreatic beta-cell regeneration in rats by (-)-epicatechin. Lancet 1981, 2:759-760.
  • [24]Chakravarthy BK, Gupta S, Gode KD: Functional beta cell regeneration in the islets of pancreas in alloxan induced diabetic rats by (-)-epicatechin. Life Sci 1982, 31:2693-2697.
  • [25]Ahmad F, Khalid P, Khan MM, Rastogi AK, Kidwai JR: Insulin like activity in (-) epicatechin. Acta Diabetol Lat 1989, 26:291-300.
  • [26]Hii CS, Howell SL: Effects of epicatechin on rat islets of Langerhans. Diabetes 1984, 33:291-296.
  • [27]Hii CS, Howell SL: Effects of flavonoids on insulin secretion and 45Ca2+ handling in rat islets of Langerhans. J Endocrinol 1985, 107:1-8.
  • [28]Sheehan EW, Stiff DD, Duah F, Slatkin DJ, Schiff PL Jr, Zemaitis MA: The lack of effectiveness of (-)-epicatechin against alloxan induced diabetes in Wistar rats. Life Sci 1983, 33:593-597.
  • [29]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. BioMed Central Full Text
  • [30]Wu LY, Juan CC, Hwang LS, Hsu YP, Ho PH, Ho LT: Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model. Eur J Nutr 2004, 43:116-124.
  • [31]Kao YH, Hiipakka RA, Liao S: Modulation of endocrine systems and food intake by green tea epigallocatechin gallate. Endocrinology 2000, 141:980-987.
  • [32]Klaus S, Pultz S, Thone-Reineke C, Wolfram S: Epigallocatechin gallate attenuates diet-induced obesity in mice by decreasing energy absorption and increasing fat oxidation. Int J Obes (Lond) 2005, 29:615-623.
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