抗阻運(yùn)動調(diào)控肥胖大鼠心肌線粒體能量代謝
發(fā)布時間:2019-06-24 10:47
【摘要】:目的:探討抗阻運(yùn)動對肥胖大鼠心肌線粒體能量代謝的影響及其分子機(jī)制。方法:Sprague-Dawley大鼠進(jìn)行8周高脂飲食后,再給予8周抗阻運(yùn)動干預(yù),檢測大鼠體重、心重以及總脂肪的重量,檢測心功能指標(biāo)、心臟脂肪酸和葡萄糖氧化率;觀測大鼠心肌線粒體結(jié)構(gòu)的改變;檢測大鼠心肌線粒體sirtuin 3(SIRT3)、長鏈脂酰輔酶A脫氫酶(long-chain acyl-Co A dehydrogenase,LCAD)和b-羥基酰基-Co A脫氫酶(b-hydroxyacyl-Co A dehydrogenase,b-HAD)的乙;突钚。結(jié)果:與高脂組相比,抗阻運(yùn)動顯著降低肥胖大鼠的體重、心重以及總脂肪的重量?棺柽\(yùn)動提高肥胖大鼠的心率、心輸出量等心功能指標(biāo),并促使心肌能量代謝底物由脂肪酸轉(zhuǎn)為葡萄糖?棺柽\(yùn)動修復(fù)肥胖誘導(dǎo)的心肌線粒體結(jié)構(gòu)紊亂?棺柽\(yùn)動顯著提高肥胖大鼠心肌SIRT3的表達(dá),降低心肌線粒體LCAD和b-HAD的乙;突钚。此外,SIRT3沉默可增加線粒體LCAD和b-HAD的乙;突钚。結(jié)論:抗阻運(yùn)動可以保護(hù)肥胖大鼠心肌線粒體結(jié)構(gòu)的完整性,調(diào)控肥胖大鼠心肌線粒體能量代謝,使脂肪酸b氧化向葡萄糖氧化轉(zhuǎn)換,改善肥胖誘導(dǎo)的心功能障礙;其機(jī)制可能與SIRT3調(diào)控線粒體LCAD和b-HAD蛋白的乙;突钚杂嘘P(guān)?棺柽\(yùn)動可作為一種行為療法,改善肥胖誘導(dǎo)的心血管并發(fā)癥。
[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.
【作者單位】: 陜西行政學(xué)院基礎(chǔ)理論教研部;
【分類號】:G804.7
本文編號:2505000
[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.
【作者單位】: 陜西行政學(xué)院基礎(chǔ)理論教研部;
【分類號】:G804.7
【相似文獻(xiàn)】
相關(guān)期刊論文 前3條
1 文安;王啟榮;方子龍;邵晶;陳成亮;周鈺杰;;急性抗阻運(yùn)動及不同比例糖和蛋白營養(yǎng)干預(yù)對男子力量項(xiàng)目運(yùn)動員尿雄激素代謝的影響[J];中國運(yùn)動醫(yī)學(xué)雜志;2012年09期
2 蘇娟,錢健 ,蔣士泉;抗阻運(yùn)動的練習(xí)方法[J];中國學(xué)校體育;2002年03期
3 王軍;陳彩珍;盧健;;耐力和抗阻運(yùn)動對血脂代謝的影響[J];福建體育科技;2008年06期
相關(guān)博士學(xué)位論文 前1條
1 文安;攝入糖—蛋白質(zhì)飲料對男性力量項(xiàng)目運(yùn)動員抗阻運(yùn)動后雄激素代謝的影響[D];上海體育學(xué)院;2012年
相關(guān)碩士學(xué)位論文 前2條
1 何苗;抗阻運(yùn)動對幼鼠骨骼肌細(xì)胞核影響的研究[D];河北師范大學(xué);2016年
2 盧貝貝;不同形式的缺血結(jié)合抗阻運(yùn)動對心臟及血管急性效應(yīng)的探討[D];南京體育學(xué)院;2016年
,本文編號:2505000
本文鏈接:http://www.sikaile.net/jiaoyulunwen/tylw/2505000.html
最近更新
教材專著