Integrative Muscle Metabolism Laboratory, Human Performance Laboratory, Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, AR, USA.
Exercise Muscle Biology Laboratory, Human Performance Laboratory, Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, AR, USA.
Acta Physiol (Oxf). 2016 Nov;218(3):167-177. doi: 10.1111/apha.12687. Epub 2016 Apr 25.
Mitochondria-encoded proteins are necessary for oxidative phosphorylation; however, no report has examined how physical activity (PA) and obesity affect mitochondrial mRNA translation machinery. Our purpose was to determine whether Western diet (WD)-induced obesity and voluntary wheel running (VWR) impact mitochondrial mRNA translation machinery and whether expression of this machinery is dictated by oxidative phenotype.
Obesity was induced with 8-wk WD feeding, and in the final 4 wks, half of mice were allowed VWR. Mitochondrial mRNA translation machinery including initiation factors (mtIF2/3), elongation factor Tu (TUFM) and translational activator (TACO1), and mitochondria-encoded proteins (CytB and ND4) was assessed by immunoblotting. The relation of mitochondrial mRNA translation to muscle oxidative phenotype was assessed using PGC-1α transgenic overexpression (MCK-PGC-1α vs. wild-type mice) and comparing across muscle groups in wild-type mice.
mtIF3 and TACO1 proteins were ~45% greater in VWR than sedentary (SED), and TACO1 and mtIF2 proteins were ~60% and 125% greater in WD than normal chow (NC). TUFM protein was ~50% lower in WD-SED than NC-SED, but ~50% greater in WD-VWR compared to NC-SED. CytB and ND4 were ~40% greater in VWR and ND4 was twofold greater with WD. TUFM, TACO1, ND4 and CytB were greater in MCK-PGC-1α compared to wild-type, and mtIF2/3 contents were not different. In oxidative muscle (soleus), mitochondrial translation machinery was elevated compared to mixed (gastrocnemius) or glycolytic (extensor digitorum longus) muscles.
These data suggest a novel mechanism promoting mitochondrial function by translation of mitochondrial protein following PA. This may act to promote muscle health by PA in obesity.
线粒体编码的蛋白质是氧化磷酸化所必需的；然而，目前尚无报道探讨体力活动（PA）和肥胖如何影响线粒体 mRNA 翻译机制。本研究旨在确定西式饮食（WD）诱导的肥胖和自愿轮跑（VWR）是否会影响线粒体 mRNA 翻译机制，以及这种机制的表达是否由氧化表型决定。
用 8 周 WD 喂养诱导肥胖，在最后 4 周，一半的小鼠被允许进行 VWR。通过免疫印迹法评估线粒体 mRNA 翻译机制，包括起始因子（mtIF2/3）、延伸因子 Tu（TUFM）和翻译激活因子（TACO1）以及线粒体编码蛋白（CytB 和 ND4）。使用过表达 PGC-1α 的转基因（MCK-PGC-1α 与野生型小鼠）和在野生型小鼠中比较不同肌肉群来评估线粒体 mRNA 翻译与肌肉氧化表型的关系。
与安静状态（SED）相比，VWR 组的 mtIF3 和 TACO1 蛋白增加了约 45%，而 WD 组的 TACO1 和 mtIF2 蛋白增加了约 60%和 125%。与 NC-SED 相比，WD-SED 组的 TUFM 蛋白减少了约 50%，但 WD-VWR 组增加了约 50%。CytB 和 ND4 在 VWR 中增加了约 40%，而 WD 中增加了两倍。与野生型相比，MCK-PGC-1α 组的 TUFM、TACO1、ND4 和 CytB 增加，而 mtIF2/3 含量没有差异。与混合（比目鱼肌）或糖酵解（伸趾长肌）肌肉相比，氧化肌肉（比目鱼肌）中的线粒体翻译机制升高。
这些数据表明，PA 后通过翻译线粒体蛋白来促进线粒体功能的新机制。这可能通过 PA 促进肥胖中的肌肉健康。
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