抗阻运动调控肥胖大鼠心肌线粒体能量代谢

发布时间：2019-06-24 10:47

【摘要】：目的:探讨抗阻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-Co A dehydrogenase,LCAD)和b-羟基酰基-Co A脱氢酶(b-hydroxyacyl-Co A dehydrogenase,b-HAD)的乙酰化和活性。结果:与高脂组相比,抗阻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。抗阻运动修复肥胖诱导的心肌线粒体结构紊乱。抗阻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,SIRT3沉默可增加线粒体LCAD和b-HAD的乙酰化和活性。结论:抗阻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。抗阻运动可作为一种行为疗法,改善肥胖诱导的心血管并发症。
[Abstract]:Objective: To study the effect of anti-blocking exercise on the energy metabolism of myocardial mitochondria in obese rats and its molecular mechanism. Methods: After 8-week high-fat diet in Sprague-Dawley rats,8-week anti-blocking exercise was given to detect the weight, heart weight and total fat weight of the rats, and the heart function index, heart fatty acid and glucose oxidation rate were detected. The ethoxylation and activity of sirtuin 3 (SIRT3), long-chain lipoxygenase A-dehydrogenase (LCAD) and b-hydroxy-base-Co A dehydrogenase (b-HAD) were detected. Results: The anti-resistance exercise significantly reduced the weight, heart weight and total fat weight of the obese rats as compared to the control group. The anti-blocking exercise can improve the heart rate, cardiac output and other cardiac function indexes of the obese rats, and promote the conversion of the energy metabolism substrate from the fatty acid to the glucose. Anti-resistance exercise is used to repair the myocardial mitochondrial structural disorder induced by obesity. The anti-blocking exercise significantly increased the expression of SIRT3 in obese rats, and decreased the ethylation and activity of the mitochondrial LCAD and b-HAD in the myocardium. In addition, SIRT3 silence can increase the ethylation and activity of mitochondrial LCAD and b-HAD. Conclusion: The anti-blocking exercise can protect the integrity of the myocardial mitochondrial structure of the obese rats, regulate the energy metabolism of the mitochondria in the myocardium of the obese rats, oxidize the fatty acid b to the glucose, and improve the cardiac function disorder induced by obesity; The mechanism may be related to the modulation and activity of mitochondrial LCAD and b-HAD proteins by SIRT3. The anti-blocking exercise can be used as an action therapy to improve the cardiovascular complications induced by obesity.
【作者单位】：陕西行政学院基础理论教研部;
【分类号】：G804.7

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