Obradovic Milan, Sudar Emina, Zafirovic Sonja, Stanimirovic Julijana, Labudovic-Borovic Milica, Isenovic Esma R
Institute Vinca, University of Belgrade, Laboratory of Radiobiology and Molecular Genetics, Belgrade, Serbia.
Institute of Histology and Embryology "Aleksandar Ð. Kostić", Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Angiology. 2015 Jan;66(1):25-35. doi: 10.1177/0003319713514477. Epub 2013 Dec 9.
We studied the in vivo effects of estradiol on size and biochemical parameters of cardiomyocytes in pathophysiological conditions such as obesity and insulin resistance. Male Wistar rats were normally fed (controls, n = 7) or fed with high-fat diet (obese, n = 14). Half of the obese rats (obese + estradiol, n = 7) were treated with a single dose of estradiol (40 μg/kg, intraperitoneally) and 24 hours after treatment all the rats were killed. Estradiol in vivo in obese rats resulted in a significant increase in protein kinase B (Akt) activation (P < .05) and decrease in heart mass (P < .05), ratio of the heart mass/body mass (P < .05), transverse diameters of cardiomyocytes (P < .001), concentration of serum high-sensitivity C-reactive protein (P < .001), and total cholesterol (P < .01) compared with obese nontreated rats. Our results suggest that estradiol in obese/IR rats affects the size of cardiomyocytes and its actions lead in vivo to a reduction in obesity-induced cardiac hypertrophy, via Akt.
我们研究了在肥胖和胰岛素抵抗等病理生理条件下,雌二醇对心肌细胞大小和生化参数的体内影响。雄性Wistar大鼠正常喂养(对照组,n = 7)或高脂饮食喂养(肥胖组,n = 14)。一半肥胖大鼠(肥胖 + 雌二醇组,n = 7)接受单剂量雌二醇(40 μg/kg,腹腔注射)治疗,治疗24小时后处死所有大鼠。与未治疗的肥胖大鼠相比,肥胖大鼠体内的雌二醇导致蛋白激酶B(Akt)激活显著增加(P < .05),心脏重量(P < .05)、心脏重量/体重比(P < .05)、心肌细胞横径(P < .001)、血清高敏C反应蛋白浓度(P < .001)和总胆固醇(P < .01)降低。我们的结果表明,肥胖/胰岛素抵抗大鼠体内的雌二醇会影响心肌细胞大小,其作用通过Akt在体内导致肥胖诱导的心脏肥大减轻。