We recently found that the mRNA expression of Slc25a25, a Ca2+-sensitive ATP carrier in the inner mitochondrial membrane, fluctuates in a circadian manner in mouse skeletal muscle. We showed here that the circadian expression of muscle Slc25a25 was damped in Clock mutant, muscle-specific Bmal1-deficient, and global Bmal1-deficient mice. Furthermore, a ketogenic diet (KD) that induces time-of-day-dependent hypothermia (torpor), induced Slc25a25 mRNA expression in skeletal muscle. Hypothermia induced by KD did not affect thermogenic genes such as Sarcolipin and Pgc1a in muscles and Ucp1 in adipose tissues. Sciatic denervation abolished circadian and KD-induced Slc25a25 expression, suggesting that the circadian clock regulates muscle Slc25a25 expression via neural pathways. We measured body temperature (Tb) in sciatic denervated mice fed with KD to determine the functional role of KD-induced Slc25a25 expression. Sciatic denervation abolished Slc25a25 expression and augmented KD-induced hypothermia compared with sham-operated mice, but did not affect Tb in mice given a normal diet. These findings suggest that KD feeding induces expression of the muscle circadian gene Slc25a25 via neural pathways, and that SLC25A25 might be involved in muscle thermogenesis under KD-induced hypothermia in mammals.

译文

:我们最近发现,线粒体内膜上的Ca2敏感ATP载体Slc25a25的mRNA表达以昼夜节律的方式在小鼠骨骼肌中波动。我们在这里显示,在Clock突变体,肌肉特异性Bmal1缺陷和整体Bmal1缺陷小鼠中,肌肉Slc25a25的昼夜节律表达受到抑制。此外,生酮饮食(KD)诱导时间依赖性低温(torpor),诱导骨骼肌中Slc25a25 mRNA表达。 KD引起的体温过低不会影响热生成基因,例如肌肉中的Sarcolipin和Pgc1a以及脂肪组织中的Ucp1。坐骨神经去神经消除了昼夜节律和KD诱导的Slc25a25表达,表明昼夜节律时钟通过神经途径调节肌肉Slc25a25的表达。我们测量了喂养KD的坐骨神经失神经小鼠的体温(Tb),以确定KD诱导的Slc25a25表达的功能作用。与假手术小鼠相比,坐骨神经失神经消除了Slc25a25的表达,并增加了KD诱导的体温过低,但在正常饮食的小鼠中并未影响Tb。这些发现表明,KD喂养通过神经途径诱导了肌肉生物节律基因Slc25a25的表达,并且SLC25A25可能参与了KD诱导的体温过低引起的哺乳动物的肌肉生热。

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