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ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #241749

Title: Green tea polyphenols improve cardiac muscle mRNA, and protein levels of signal pathways related to insulin and lipid metabolism and inflammation in insulin-resistant rats

Author
item QIN, BOLIN - Integrity Neutraceuticals
item Polansky, Marilyn
item Dawson, Harry
item Anderson, Richard

Submitted to: Molecular Nutrition and Food Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/20/2009
Publication Date: 5/1/2010
Citation: Qin, B., Polansky, M.M., Dawson, H.D., Anderson, R.A. 2010. Green tea polyphenols improve cardiac muscle mRNA, and protein levels of signal pathways related to insulin and lipid metabolism and inflammation in insulin-resistant rats. Molecular Nutrition and Food Research. 54(S1)S14-S23.

Interpretive Summary: Green tea may exert multiple effects on human health. Epidemiologic studies indicate that consumption of green tea may reduce the risk of coronary artery disease and harmful cardiac events. To explore potential underlying mechanisms of action at the molecular level, we examined the effects of an extract of green tea on proteins responding to genes involved in insulin activity, fat metabolism, and inflammation. In rats fed a high-fructose diet to induce early signs of diabetes and cardiovascular disease, supplementation with the green tea extract for 6 weeks reduced blood glucose, plasma insulin levels, proteins involved in the control of fat levels, cholesterol, triglycerides, free fatty acids, and LDL cholesterol levels, as well as inflammatory factors. Green tea did not affect food intake, body weight, or heart weight, but improved factors related to insulin function and fat metabolism, and decreased inflammatory factors in the heart. In summary, consumption of green tea extract ameliorated the detrimental effects of eating a diet high in fructose on insulin activity, fat metabolism, and inflammation in rats. This study will be of benefit to scientists working on the causes of cardiovascular diseases associated with abnormal insulin function, and potentially to the millions of people with diabetes and cardiovascular diseases.

Technical Abstract: Epidemiologic studies indicate that the consumption of green tea polyphenols (GTP) may reduce the risk of coronary artery disease. To explore the underlying mechanisms of action at the molecular level, we examined the effects of GTP on cardiac mRNA and protein levels of genes involved in insulin and lipid metabolism and inflammation. In rats fed a high-fructose diet (HFD), supplementation with GTP (200 mg/kg BW daily dissolved in distilled water) for 6 wk reduced levels of systemic blood glucose, plasma insulin, retinol binding protein 4 (RBP4), soluble CD36 (sCD36), cholesterol, triglycerides, free fatty acids, and LDL-cholesterol, as well as gene expression for the pro-inflammatory cytokines TNF-a and IL-6. GTP did not affect food intake, body weight, or heart weight. In the myocardium, GTP increased mRNA expression for the insulin receptor (Ir), insulin receptor substrate 1 (Irs1), Irs2, phosphoinositide-3-kinase (PI3k), v-akt murine thymoma viral oncogene homolog 1 (Akt1), glucose transporter 1 (Glut1), Glut4, and glycogen synthase 1 (Gys1), but inhibited phosphatase and tensin homolog deleted on chromosome ten (Pten) expression, and decreased glycogen synthase kinase 3ß (Gsk3ß) expression. The sterol regulatory element binding protein-1c (Srebp1c) mRNA, microsomal triglyceride transfer protein (Mttp) mRNA and protein, and Cd36 mRNA and protein levels were decreased, and peroxisome proliferator-activated receptor(PPAR)Gamma mRNA levels were increased. GTP also decreased mRNA expression for the inflammatory factors Tnf, Il1b, and Il6, and enhanced protein and mRNA expression of the anti-inflammatory zinc finger protein (Zfp)36. In summary, consumption of GTP ameliorated the detrimental effects of HFD on insulin signaling, lipids, and inflammation in rats.