Vitamin C deficiency causes muscle atrophy and a deterioration in physical performance.
Vitamin C deficiency causes muscle atrophy and a deterioration in physical performance.
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维生素C缺乏会导致肌肉萎缩和身体机能下降。
DOI：
10.1038/s41598-019-41229-7
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
and Ishigami. A
中科院分区：
文献类型：
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作者：
Takizawa;S.;Funakoshi;T.;Yatsu;T.;Nagata;K.;Aigaki;T.;Machida;S.;and Ishigami. A
L-抗坏血酸（AsA）是一种水溶性抗氧化剂。我们使用 AsA 生物合成缺陷的衰老标记蛋白 30 (SMP30) 敲除 (KO) 小鼠（这使得该小鼠模型与人类相似）检查了 AsA 缺乏对骨骼肌的影响，以阐明 AsA 在骨骼肌中的功能。将八周龄雌性 SMP30-KO 小鼠分为以下两组：给予 AsA 充足组 [AsA(+)]，给予 1.5 g/L AsA；给予 AsA 缺乏组 [AsA(−)]，给予自来水（不含 AsA）水。 4周时，AsA(-)小鼠腓肠肌中的AsA含量比AsA(+)小鼠腓肠肌中的AsA含量低0.7%。在 12 周和 16 周时，AsA(-) 小鼠的所有肌肉重量均显着低于 AsA(+) 小鼠。 16周时AsA(-)小鼠的比目鱼肌横截面积明显小于AsA(+)小鼠。 12周时AsA(-)小鼠的体能明显低于AsA(+)小鼠。 AsA 缺乏 12 周后，泛素连接酶的表达上调，例如 atrogin1/肌肉萎缩 F-box (MAFbx) 和肌肉环指蛋白 1 (MuRF1)。此外，在补充 AsA 12 周后，在 12 周时检测到的所有 AsA 缺乏对 AsA(−) 组肌肉的影响均得到恢复。因此，长期的 AsA 缺乏与肌肉萎缩有关，这可以通过恢复 AsA 水平来逆转。
L-Ascorbic acid (AsA) is a water-soluble antioxidant. We examined the effect of AsA deficiency on skeletal muscle using senescence marker protein-30 (SMP30)-knockout (KO) mice that are defective in AsA biosynthesis, which makes this mouse model similar to humans, to clarify the function of AsA in skeletal muscle. Eight-week-old female SMP30-KO mice were divided into the following two groups: an AsA-sufficient group [AsA(+)] that was administered 1.5 g/L AsA and an AsA-deficient group [AsA(−)] that was administered tap (AsA-free) water. At 4 weeks, the AsA content in the gastrocnemius muscle of AsA(−) mice was 0.7% compared to that in the gastrocnemius muscle of AsA(+) mice. Significantly lower weights of all muscles were observed in AsA(−) mice than those in AsA(+) mice at 12 and 16 weeks. The cross-sectional area of the soleus was significantly smaller in AsA(−) mice at 16 weeks than that in AsA(+) mice. The physical performance of AsA(−) mice was significantly less than that of AsA(+) mice at 12 weeks. Following AsA deficiency for 12 weeks, the expression of ubiquitin ligases, such as atrogin1/muscle atrophy F-box (MAFbx) and muscle RING-finger protein 1 (MuRF1), was upregulated. Furthermore, all detected effects of AsA deficiency on muscles of the AsA(−) group at 12 weeks were restored following AsA supplementation for 12 weeks. Thus, longer-term AsA deficiency is associated with muscle wasting, that this can be reversed by restoring AsA levels.