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首页> 外文期刊>FEBS letters. >Acute administration of 3,5-diiodo-l-thyronine to hypothyroid rats affects bioenergetic parameters in rat skeletal muscle mitochondria.
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Acute administration of 3,5-diiodo-l-thyronine to hypothyroid rats affects bioenergetic parameters in rat skeletal muscle mitochondria.

机译:对甲状腺功能减退的大鼠急性给予3,5-二碘-1-甲状腺素会影响大鼠骨骼肌线粒体的生物能参数。

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摘要

We investigated the mechanism by which 3,5-diiodo-l-thyronine (T2) affects skeletal muscle mitochondrial bioenergetic parameters following its acute administration to hypothyroid rats. One hour after injection, T2 increased both coupled and uncoupled respiration rates by +27% and +42%, respectively. Top-down elasticity analysis revealed that these effects were the result of increases in the substrate oxidation and mitochondrial uncoupling. Discriminating between proton-leak and redox-slip processes, we identified an increased mitochondrial proton conductance as the "pathway" underlying the effect of T2 on mitochondrial uncoupling. As a whole, these results may provide a mechanism by which T2 rapidly affects energy metabolism in hypothyroid rats.
机译:我们调查了3,5-二碘-1-胸腺嘧啶(T2)对甲状腺功能减退大鼠急性给药后影响骨骼肌线粒体生物能参数的机制。注射后一小时,T2分别使耦合和非耦合呼吸率分别增加了+ 27%和+ 42%。自上而下的弹性分析表明,这些影响是底物氧化和线粒体解偶联增加的结果。区分质子泄漏和氧化还原滑动过程,我们确定线粒体质子电导的增加是“ T2对线粒体解偶联作用的基础”。总体而言,这些结果可提供一种机制,通过该机制T2可以快速影响甲状腺功能减退大鼠的能量代谢。

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