Lombardi Assunta, Lanni Antonia, de Lange Pieter, Silvestri Elena, Grasso Paola, Senese Rosalba, Goglia Fernando, Moreno Maria
Dipartimento delle Scienze Biologiche, Sezione Fisiologia ed Igiene, Universitá degli Studi di Napoli Federico II, Via Mezzocannone, 8 80134 Napoli, Italy.
FEBS Lett. 2007 Dec 22;581(30):5911-6. doi: 10.1016/j.febslet.2007.11.073. Epub 2007 Dec 3.
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.
我们研究了对甲状腺功能减退大鼠急性给予3,5-二碘-L-甲状腺原氨酸（T2）后，T2影响骨骼肌线粒体生物能量参数的机制。注射后1小时，T2使偶联呼吸率和非偶联呼吸率分别增加了27%和42%。自上而下的弹性分析表明，这些效应是底物氧化和线粒体解偶联增加的结果。通过区分质子泄漏和氧化还原滑移过程，我们确定线粒体质子传导增加是T2对线粒体解偶联作用的“途径”。总体而言，这些结果可能提供了一种机制，通过该机制T2可快速影响甲状腺功能减退大鼠的能量代谢。
