Department of General Pediatrics, Center for Paediatrics and Adolescent Medicine, Faculty of Medicine and Medical Centre, University of Freiburg, Germany.
Core Facility Proteomics, Center for Biological Systems Analysis (ZBSA), University of Freiburg, Germany.
FEBS Lett. 2018 Jan;592(2):219-232. doi: 10.1002/1873-3468.12940. Epub 2018 Jan 4.
The white skeletal muscle of very long-chain acyl-CoA-dehydrogenase-deficient (VLCAD ) mice undergoes metabolic modification to compensate for defective β-oxidation in a progressive and time-dependent manner by upregulating glucose oxidation. This metabolic regulation seems to be accompanied by morphologic adaptation of muscle fibers toward the glycolytic fiber type II with the concomitant upregulation of mitochondrial fatty acid biosynthesis (mFASII) and lipoic acid biosynthesis. Dietary supplementation of VLCAD mice with different medium-chain triglycerides over 1 year revealed that odd-chain species has no effect on muscle fiber switch, whereas even-chain species inhibit progressive metabolic adaptation. Our study shows that muscle may undergo adaptive mechanisms that are modulated by dietary supplementation. We describe for the first time a concomitant change of mFASII in this muscular adaptation process.
非常长链酰基辅酶 A 脱氢酶缺乏症（VLCAD）小鼠的白色骨骼肌通过上调葡萄糖氧化作用，以渐进和时间依赖的方式发生代谢修饰，从而补偿β-氧化缺陷。这种代谢调节似乎伴随着肌纤维向糖酵解纤维类型 II 的形态适应，同时伴随着线粒体脂肪酸生物合成（mFASII）和硫辛酸生物合成的上调。用不同的中链甘油三酯对 VLCAD 小鼠进行为期 1 年的饮食补充表明，奇数链物种对肌纤维转换没有影响，而偶数链物种则抑制渐进的代谢适应。我们的研究表明，肌肉可能会发生适应性机制，这些机制受饮食补充的调节。我们首次描述了在这种肌肉适应过程中 mFASII 的伴随变化。
