Basal and resistance exercise-induced increase in protein synthesis is impaired in skeletal muscle of iron-deficient rats.
Basal and resistance exercise-induced increase in protein synthesis is impaired in skeletal muscle of iron-deficient rats.
复制标题
缺铁大鼠的骨骼肌中，基础运动和抗阻运动引起的蛋白质合成增加受到损害。
DOI：
10.1016/j.nut.2021.111389
复制
发表时间：
2021
期刊：
影响因子：
4.4
通讯作者：
Nakai N.
中科院分区：
文献类型：
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作者：
Higashida K;Inoue S;Takeuchi N;Ato S;Ogasawara R;Nakai N.
目的探讨铁缺乏对基础和收缩引起的肌肉蛋白质合成增加的影响。方法4周龄雄性sd大鼠分为3组。三组中有两组的大鼠在4周内自由食用控制饮食（AD）或缺铁饮食（ID）。第三组（CON）按ID组的平均摄取量饲喂对照饲料。结果与CON组比较，ID组骨骼肌红细胞压积、血红蛋白浓度、含铁蛋白水平和总铁含量显著低于CON组，而非含铁蛋白水平组间无显著差异。用嘌呤霉素标记肽测量的蛋白质合成，在基础状态和收缩刺激状态下，与CON组相比，ID组的蛋白质合成都较低。低脂饮食损害了参与蛋白质合成的信号通路的激活水平，如核糖体蛋白S6和真核翻译起始因子4e结合蛋白1。此外，缺铁降低了自噬能力，但不影响泛素化蛋白含量。这些结果表明，严重缺铁不仅减少了基础，而且减少了肌肉收缩引起的蛋白质合成增加，至少部分原因是骨骼肌中蛋白质合成信号通路的下调。
ObjectivesWe aimed to investigate the effect of iron deficiency on basal- and contraction-induced increases in muscle protein synthesis.MethodsFour-wk-old male Sprague–Dawley rats were divided into three groups. The rats in two of the three groups had free access to a control diet (AD) or iron-deficient diet (ID) for 4 wk. The rats in the third group (CON) were pair-fed the control diet to the mean intake of the ID group.ResultsIn comparison with the CON group, the ID group showed significantly lower hematocrit and hemoglobin concentrations, iron-containing protein levels, and total iron content in skeletal muscle, but non-iron-containing protein levels did not show any differences between the groups. Protein synthesis, measured by puromycin-labeled peptides, was lower in the ID group compared with the CON group in both basal- and contraction-stimulated states. The ID diet impaired the activation levels of signaling pathways involved in protein synthesis, such as ribosomal protein S6 and eukaryotic translation initiation factor 4E-binding protein 1. Furthermore, dietary iron deficiency decreased autophagy capacity, but did not affect the ubiquitinated protein content.ConclusionsThese results suggest that severe iron deficiency decreases not only basal but also muscle contraction-induced increases in protein synthesis due to, at least in part, downregulation of the protein synthesis signaling pathway in the skeletal muscle.