运动引起的葡萄糖代谢变化促进心脏生理生长
Andrew A Gibb1,2,3, Paul N Epstein4, Shizuka Uchida5
1Institute of Molecular Cardiology (A.A.G., Y.Z., L.A.M., K.K., P.T., D.J.C., K.R.B., S.P.J., A.B., B.G.H.).
Circulation
|September 2, 2017
概括
运动引起的心脏糖解降低促进心脏生理生长. 代谢灵活性对于保持心脏线粒体健康和功能至关重要.
科学领域:
- 心血管生理学
- 代谢调节
- 心脏重塑
背景情况:
- 运动诱导了与生理心脏生长相关的心脏代谢重塑.
- 身体活动影响心脏代谢和重塑的确切机制尚不清楚.
研究的目的:
- 调查心肌细胞葡萄糖代谢的运动变化是否对心脏生理生长至关重要.
- 阐明糖解活性在运动诱导的心脏重塑中的作用.
主要方法:
- 在接受跑步机运动的小鼠中进行放射学,免疫学,代谢学和生物化学测定.
- 评估突变性6-果糖-2-激酶/果糖-2,6-双酸酶 (PFKFB) 的心脏特异性表达,以调节糖解活性.
- 代谢和转录分析以确定受调节的途径和基因组.
主要成果:
- 运动急剧降低了糖分分解,但在适应时增加了,调节了果酶 (PFK) 的活性.
- 降低糖解 (GlycoLo小鼠) 增强了心脏功能,肌细胞大小和毛细血管对肌细胞的比率.
- 改变的PFKFB活动影响了葡萄糖 - 脂肪酸循环,不灵活导致线粒体损伤;糖解调节心脏重塑基因.
结论:
- 运动诱导的心脏糖溶解减少刺激心脏生理重塑.
- 代谢灵活性对于保持心脏线粒体健康至关重要.
- 糖解活性是心脏新陈代谢和基因改造程序的关键调节者.
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