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适度耐力运动对肥胖大鼠心脏端粒和心血管重塑的影响。

The impact of moderate endurance exercise on cardiac telomeres and cardiovascular remodeling in obese rats.

作者信息

Semeraro Maria Donatella, Beltrami Antonio Paolo, Kharrat Feras, Almer Gunter, Sedej Simon, Renner Wilfried, Gruber Hans-Jürgen, Curcio Francesco, Herrmann Markus

机构信息

Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria.

Department of Medicine (DAME), University of Udine, Udine, Italy.

出版信息

Front Cardiovasc Med. 2023 Jan 6;9:1080077. doi: 10.3389/fcvm.2022.1080077. eCollection 2022.

Abstract

INTRODUCTION

Hypercaloric nutrition and physical inactivity cause obesity, a potential driver of myocardial apoptosis and senescence that may accelerate cardiac aging. Although physical activity reduces mortality, its impact on myocardial aging is insufficiently understood. Here we investigated the effects of a hypercaloric high-fat diet (HFD) and regular exercise training on cardiac cells telomeres and histomorphometric indices of cardiac aging.

METHODS

Ninety-six 4-months old female Sprague-Dawley rats were fed for 10 months normal (ND) or a HFD diet. Half of the animals in each group performed 30 min treadmill-running sessions on 5 consecutive days per week. At study end, cardiomyocyte cross-sectional area (CSA), interstitial collagen content, vascular density, apoptotic and senescent cells, relative telomere length (RTL), and expression of telomerase-reverse transcriptase () as marker of telomere-related senescence and apoptosis were analyzed.

RESULTS

Compared to ND, the HFD group developed obesity, higher CSA, lower capillary density and tended to have more apoptotic cardiomyocytes and interstitials cells. Myocardial RTL and the expression of and were comparable in sedentary HFD and ND animals. In the HFD group, regular moderate endurance exercise improved myocardial vascularization, but had no effect on CSA or apoptosis. Notably, the combination of exercise and HFD increased senescence when compared to sedentary ND or HFD, and reduced RTL when compared to exercise ND animals. Exercising HFD animals also showed a trend toward higher expression compared to all other groups. In addition, exercise reduced expression regardless of diet.

CONCLUSION

HFD-induced obesity showed no effects on myocardial telomeres and induced only mild morphologic alterations. Summarized, long-term moderate endurance exercise partially reverses HFD-induced effects but may even trigger cardiac remodeling in the context of obesity.

摘要

引言

高热量营养和缺乏体育活动会导致肥胖,而肥胖是心肌细胞凋亡和衰老的潜在驱动因素,可能会加速心脏衰老。尽管体育活动可降低死亡率,但其对心肌衰老的影响仍未得到充分了解。在此,我们研究了高热量高脂肪饮食(HFD)和规律运动训练对心脏细胞端粒及心脏衰老组织形态学指标的影响。

方法

将96只4月龄雌性Sprague-Dawley大鼠分为两组,分别给予正常饮食(ND)或HFD饮食,持续喂养10个月。每组动物中一半每周连续5天进行30分钟的跑步机跑步训练。在研究结束时,分析心肌细胞横截面积(CSA)、间质胶原含量、血管密度、凋亡和衰老细胞、相对端粒长度(RTL)以及作为端粒相关衰老和凋亡标志物的端粒酶逆转录酶()的表达。

结果

与ND组相比,HFD组出现肥胖,CSA更高,毛细血管密度更低,且凋亡心肌细胞和间质细胞数量有增加趋势。久坐不动的HFD组和ND组动物的心肌RTL以及和的表达相当。在HFD组中,规律的适度耐力运动改善了心肌血管生成,但对CSA或凋亡无影响。值得注意的是,与久坐不动的ND组或HFD组相比,运动与HFD相结合会增加衰老,与运动的ND组动物相比会降低RTL。与所有其他组相比,运动的HFD组动物的表达也有升高趋势。此外,无论饮食如何,运动均可降低表达。

结论

HFD诱导的肥胖对心肌端粒无影响,仅引起轻度形态学改变。总之,长期适度耐力运动可部分逆转HFD诱导的影响,但在肥胖情况下甚至可能引发心脏重塑。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e03/9853517/0d08ae03eb6c/fcvm-09-1080077-g0001.jpg

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