黎茜.抗阻力运动调控肥胖大鼠心肌线粒体能量代谢[J].北京体育大学学报,2017,40(9):48-53.
抗阻力运动调控肥胖大鼠心肌线粒体能量代谢
Resistance Training Regulates Myocardial Mitochondrial Energy Metabolism on Obese Rats
投稿时间:2017-01-30  
DOI:10.19582/j.cnki.11-3785/g8.2017.09.008
中文关键词:  关键词:抗阻力运动  肥胖  心肌  线粒体能量代谢。
英文关键词:Keywords: resistance training  obesity  myocardium  mitochondrial energy metabolism.
基金项目:
作者单位
黎茜 陕西行政学院基础理论教研部陕西 西安 710068 
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中文摘要:
      摘要:目的:探讨抗阻力运动对肥胖大鼠心肌线粒体能量代谢的影响及其分子机制。方法:Sprague-Dawley大鼠进行8周高脂饮食后,再给予8周抗阻力运动干预,检测大鼠体重、心重以及总脂肪的重量,检测心功能指标、心脏脂肪酸和葡萄糖氧化率。观测大鼠心肌线粒体结构的改变。检测大鼠心肌线粒体sirtuin 3(SIRT3)、长链脂酰辅酶A脱氢酶(long-chain acyl-CoA dehydrogenase, LCAD) 和b-羟基酰基-CoA脱氢酶(b-hydroxyacyl-CoA dehydrogenase, b-HAD)的乙酰化和活性。结果:与高脂组相比,抗阻力运动显著降低肥胖大鼠的体重、心重以及总脂肪的重量。抗阻力运动提高肥胖大鼠的心率、心输出量等心功能指标,并促使心肌能量代谢底物由脂肪酸转为葡萄糖。抗阻力运动修复肥胖诱导的心肌线粒体结构紊乱。抗阻力运动显著提高肥胖大鼠心肌SIRT3的表达,降低心肌线粒体LCAD和b-HAD的乙酰化和活性。此外,正常大鼠心肌细胞的体外研究表明,SIRT3沉默可增加线粒体LCAD和b-HAD的乙酰化和活性。结论:抗阻力运动可以保护肥胖大鼠心肌线粒体结构的完整性,调控肥胖大鼠心肌线粒体能量代谢,使脂肪酸b氧化向葡萄糖氧化转换,改善肥胖诱导的心功能障碍。其机制可能与SIRT3调控线粒体LCAD和b-HAD蛋白的乙酰化和活性有关。抗阻力运动可作为一种行为疗法,改善肥胖诱导的心血管并发症。
英文摘要:
      Abstract: Objective: To explore the effect of resistance training on myocardial mitochondrial energy metabolism of obese rats and its underlying mechanisms. Methods: After 8 weeks high-fat diet (HFD), the rats preformed resistance training program, and their body weight, heart weight and total fat weight were measured, their parameters of cardiac function, oxidation rates of fatty acid and glucose were tested, and the myocardial mitochondrial structure was observed; the acetylation and activity of SIRT3, LCAD and b-HAD in myocardial mitochondria of rats were measured. Results: Compared with HFD group, the body weight, heart weight and total fat mass of resistance training group rats dramatically reduced, their cardiac function including heart rate, cardiac output and cardiac work increased, and their substrate for myocardial energy metabolism was converted from fatty acids to glucose. Resistance training could repair obesity-induced structure disturbance of myocardial mitochondria in rats, significantly increase SIRT3 expression in myocardium, decreased acetylation and activity of LCAD and b-HAD in myocardial mitochondria. In vitro study of normal rat cardiomyocytes, SIRT3 silencing could increase acetylation and activity of LCAD and b-HAD in mitochondria. Conclusions: Resistance training can protect structural integrality of myocardial mitochondria of obese rats, regulate rats’ myocardial mitochondrial energy metabolism, transform fatty acid oxidation into glucose oxidation, and alleviate obesity-induced cardiac dysfunction. And its underlying mechanism may be associated with regulation of SIRT3 on acetylation and activity of LCAD and b-HAD in myocardial mitochondria. Resistance training can be used as a behavior therapy to improve obesity-induced cardiovascular complication.
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