Green tea polyphenol extract regulates the expression of genes involved in glucose uptake and insulin signaling in rats fed a high fructose diet

被引:114
作者
Cao, Heping
Hininger-Favier, Isabelle
Kelly, Meghan A.
Benaraba, Rachida
Dawson, Harry D.
Coves, Sara
Roussel, Anne M.
Anderson, Richard A.
机构
[1] USDA, Beltsville Human Nutr Res Ctr, Agr Res Serv, Nutrient Requirements & Funct Lab, Baltimore, MD 20705 USA
[2] Univ Grenoble 1, Fac Pharm, Lab NVMC, F-92842 Rueil Malmaison, France
关键词
diabetes; fructose-rich diet; green tea; glucose transporter; insulin signaling pathway; obesity; polyphenol extract; rat;
D O I
10.1021/jf070695o
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Green tea has antidiabetic, antiobesity, and anti-inflammatory activities in animal models, but the molecular mechanisms of these effects have not been fully understood. Quantitative real-time polymerase chain reaction (PCR) was used to investigate the relative expression levels and the effects of green tea (1 and 2 g solid extract/kg diet) on the expression of glucose transporter family genes (Glut1/Slc2a1, Glut2/Slc2a2, Glut3/Slc2a3, and Glut4/Slc2a4) and insulin signaling pathway genes (Ins1, Ins2, Insr, Irs1, Irs2, Akt1, Grb2, Igf1, Igf2, Igf1r, Igf2r, Gsk3b, Gys1, Pik3cb, Pik3r1, Shc1, and Sos1) in liver and muscle of rats fed a high-fructose diet known to induce insulin resistance and oxidative stress. Glut2 and Glut4 were the major Glut mRNAs in rat liver and muscle, respectively. Green tea extract (1 g) increased Glut1, Glut4, Gsk3b, and Irs2 mRNA levels by 110, 160, 30, and 60% in the liver, respectively, and increased Irs1 by 80% in the muscle. Green tea extract (2 g) increased Glut4, Gsk3b, and Pik3cb mRNA levels by 90, 30, and 30% but decreased Shc1 by 60% in the liver and increased Glut2, Glut4, Shc1, and Sos1 by 80, 40, 60, and 50% in the muscle. This study shows that green tea extract at 1 or 2 g/kg diet regulates gene expression in the glucose uptake and insulin signaling pathway in rats fed a fructose-rich diet.
引用
收藏
页码:6372 / 6378
页数:7
相关论文
共 51 条
[41]   Green tea catechin, epigallocatechin-3-gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex [J].
Rodriguez, SK ;
Guo, WM ;
Liu, LP ;
Band, MA ;
Paulson, EK ;
Meydani, M .
INTERNATIONAL JOURNAL OF CANCER, 2006, 118 (07) :1635-1644
[42]   Effects of green tea consumption on inflammation, insulin resistance and pulse wave velocity in type 2 diabetes patients [J].
Ryu, OH ;
Lee, J ;
Lee, KW ;
Kim, HY ;
Seo, JA ;
Kim, SG ;
Kim, NH ;
Baik, SH ;
Choi, DS ;
Choi, KM .
DIABETES RESEARCH AND CLINICAL PRACTICE, 2006, 71 (03) :356-358
[43]   Mechanisms of disease - Glucose transporters and insulin action - Implications for insulin resistance and diabetes mellitus [J].
Shepherd, PR ;
Kahn, BB .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 341 (04) :248-257
[44]   Type 2 diabetes: principles of pathogenesis and therapy [J].
Stumvoll, M ;
Goldstein, BJ ;
van Haeften, TW .
LANCET, 2005, 365 (9467) :1333-1346
[45]   The insulin signaling pathway [J].
Taha, C ;
Klip, A .
JOURNAL OF MEMBRANE BIOLOGY, 1999, 169 (01) :1-12
[46]   Insulin and insulin-like growth factor I up-regulate GLUT4 gene expression in fetal brown adipocytes, in a phosphoinositide 3-kinase-dependent manner [J].
Valverde, AM ;
Navarro, P ;
Teruel, T ;
Conejo, R ;
Benito, M ;
Lorenzo, M .
BIOCHEMICAL JOURNAL, 1999, 337 :397-405
[47]   Anti-obesity effects of green tea: From bedside to bench [J].
Wolfram, S ;
Wang, Y ;
Thielecke, F .
MOLECULAR NUTRITION & FOOD RESEARCH, 2006, 50 (02) :176-187
[48]   Effect of green tea supplementation on insulin sensitivity in Sprague-Dawley rats [J].
Wu, LY ;
Juan, CC ;
Ho, LT ;
Hsu, YP ;
Hwang, LS .
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2004, 52 (03) :643-648
[49]   Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model [J].
Wu, LY ;
Juan, CC ;
Hwang, LS ;
Hsu, YP ;
Ho, PH ;
Ho, LT .
EUROPEAN JOURNAL OF NUTRITION, 2004, 43 (02) :116-124
[50]   Inhibition of carcinogenesis by dietary polyphenolic compounds [J].
Yang, CS ;
Landau, JM ;
Huang, MT ;
Newmark, HL .
ANNUAL REVIEW OF NUTRITION, 2001, 21 :381-406