PMID- 20112301 OWN - NLM STAT- MEDLINE DCOM- 20100913 LR - 20171116 IS - 1613-4133 (Electronic) IS - 1613-4125 (Linking) VI - 54 Suppl 1 DP - 2010 May TI - 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. PG - S14-23 LID - 10.1002/mnfr.200900306 [doi] AB - Epidemiological 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 the cardiac mRNA and protein levels of genes involved in insulin and lipid metabolism and inflammation. In rats fed a high-fructose diet, supplementation with GTP (200 mg/kg BW daily dissolved in distilled water) for 6 wk, reduced systemic blood glucose, plasma insulin, retinol-binding protein 4, soluble CD36, cholesterol, triglycerides, free fatty acids and LDL-C levels, as well as the pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and IL-6. GTP did not affect food intake, bodyweight and heart weight. In the myocardium, GTP also increased the insulin receptor (Ir), insulin receptor substrate 1 and 2 (Irs1 and Irs2), phosphoinositide-3-kinase (Pi3k), v-akt murine thymoma viral oncogene homolog 1 (Akt1), glucose transporter 1 and 4 (Glut1 and Glut4) and glycogen synthase 1 (Gys1) expression but inhibited phosphatase and tensin homolog deleted on chromosome ten (Pten) expression and decreased glycogen synthase kinase 3beta (Gsk3beta) mRNA expression. The sterol regulatory element-binding protein-1c (Srebp1c) mRNA, microsomal triglyceride transfer protein (Mttp) mRNA and protein, Cd36 mRNA and cluster of differentiation 36 protein levels were decreased and peroxisome proliferator-activated receptor (Ppar)gamma mRNA levels were increased. GTP also decreased the inflammatory factors: Tnf, Il1b and Il6 mRNA levels, and enhanced the anti-inflammatory protein, zinc-finger protein, protein and mRNA expression. In summary, consumption of GTP ameliorated the detrimental effects of high-fructose diet on insulin signaling, lipid metabolism and inflammation in the cardiac muscle of rats. FAU - Qin, Bolin AU - Qin B AD - Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, MD 20705, USA. FAU - Polansky, Marilyn M AU - Polansky MM FAU - Harry, Dawson AU - Harry D FAU - Anderson, Richard A AU - Anderson RA LA - eng PT - Journal Article PT - Research Support, U.S. Gov't, Non-P.H.S. PL - Germany TA - Mol Nutr Food Res JT - Molecular nutrition & food research JID - 101231818 RN - 0 (Blood Glucose) RN - 0 (CD36 Antigens) RN - 0 (Flavonoids) RN - 0 (Insulin) RN - 0 (Muscle Proteins) RN - 0 (Phenols) RN - 0 (Polyphenols) RN - 0 (RNA, Messenger) RN - 0 (Rbp4 protein, rat) RN - 0 (Retinol-Binding Proteins, Plasma) RN - 0 (Tea) RN - 86-01-1 (Guanosine Triphosphate) RN - EC 2.7.11.1 (GSK3B protein, human) RN - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta) RN - EC 2.7.11.1 (Gsk3b protein, rat) RN - EC 2.7.11.26 (Glycogen Synthase Kinase 3) SB - IM MH - Animals MH - Blood Glucose/metabolism MH - Body Weight/drug effects MH - CD36 Antigens/blood MH - Flavonoids/*pharmacology MH - Gene Deletion MH - Gene Expression Regulation/drug effects MH - Glycogen Synthase Kinase 3/genetics MH - Glycogen Synthase Kinase 3 beta MH - Guanosine Triphosphate/pharmacology MH - Inflammation/prevention & control MH - Insulin/blood MH - Insulin Resistance/*physiology MH - Muscle Proteins/*metabolism MH - Myocardium/*metabolism MH - Organ Size/drug effects MH - Phenols/*pharmacology MH - Polyphenols MH - RNA, Messenger/*genetics/metabolism MH - Rats MH - Retinol-Binding Proteins, Plasma/metabolism MH - *Tea EDAT- 2010/01/30 06:00 MHDA- 2010/09/14 06:00 CRDT- 2010/01/30 06:00 PHST- 2010/01/30 06:00 [entrez] PHST- 2010/01/30 06:00 [pubmed] PHST- 2010/09/14 06:00 [medline] AID - 10.1002/mnfr.200900306 [doi] PST - ppublish SO - Mol Nutr Food Res. 2010 May;54 Suppl 1:S14-23. doi: 10.1002/mnfr.200900306.