17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

被引:13
作者
Zafirovic, Sonja [1 ]
Obradovic, Milan [1 ]
Sudar-Milovanovic, Emina [1 ]
Jovanovic, Aleksandra [1 ]
Stanimirovic, Julijana [1 ]
Stewart, Alan J. [2 ]
Pitt, Samantha J. [2 ]
Isenovic, Esma R. [1 ]
机构
[1] Univ Belgrade, Inst Nucl Sci Vinca, Lab Radiobiol & Mol Genet, Mike Petrovica Alasa 12-14, Belgrade 11000, Serbia
[2] Univ St Andrews, Sch Med, St Andrews KY16 9TF, Fife, Scotland
关键词
Estradiol; Obesity; Myocardial metabolism; Cardiovascular diseases; Inducible nitric oxide synthase; INDUCED INSULIN-RESISTANCE; FRUCTOSE-RICH DIET; OBESE ZUCKER RATS; ESTROGEN-RECEPTOR; IN-VIVO; ACID TRANSPORTERS; SKELETAL-MUSCLE; NA+/K+-ATPASE; L-ARGININE; ER-ALPHA;
D O I
10.1016/j.mce.2017.02.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The aim of this study was to investigate the in vivo effects of 17 beta-estradiol (E-2) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. Male Wistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E-2 while the other half were placebo-treated. 24 h after treatment animals were sacrificed. E-2 reduced cardiac free fatty acid (FFA) (p < 0.05), L-arginine (p < 0.01), iNOS mRNA (p < 0.01), and protein (p < 0.05) levels and translocation of the FFA transporter (CD36) (p < 0.01) to the plasma membrane (PM) in HF fed rats. In contrast, Akt phosphorylation at Thr308 (p < 0.05) and translocation of the glucose transporter GLUT4 (p < 0.05) to the PM increased after E-2 treatment in HF rats. Our results indicate that E-2 acts via the PI3K/Akt signalling pathway to partially protect myocardial metabolism by attenuating the detrimental effects of increased iNOS expression/activity in HF fed rats. (C) 2017 Elsevier B.V. All rights reserved.
引用
收藏
页码:12 / 20
页数:9
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