Vitamin C Deficiency Causes Muscle Atrophy and a Deterioration in Physical Performance
Open accessAbstract
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.
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Vitamin C deficiency causes muscle atrophy in mice, associated with high expression of MAFbx and MuRF1 and overproduction of ROS.
“Vitamin C deficiency causes muscle atrophy in mice, which is associated with high expression of muscle atrophy gene of MAFbx and MuRF1 and overproduction of ROS.”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [56]
Muscle atrophy in vitamin C deficient mice was restored by 12 weeks of vitamin C supplementation.
“The muscle atrophy was restored by 12 weeks of vitamin C supplementation [56].”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [56]
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- Authors
- Takisawa, S., Funakoshi, T., Yatsu, T., Nagata, K., Aigaki, T., Machida, S., & Ishigami, A.
- Affiliations
- Toho University (JP)
- Tokyo Metropolitan Institute of Gerontology (JP)
- Tokyo Metropolitan University (JP)
- Juntendo University (JP)
- Corresponding author
- Ishigami, Akihito
- Venue
- Scientific Reports
- Published
- 2019-03-20
- Volume
- 9
- Issue
- 1
- Pages
- 4702-4702
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6426981
- OpenAlex
- W2923144925
- Cited by
- 63
- References
- 41
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 14 · 2023: 9 · 2022: 11 · 2021: 4 · 2020: 8
- FWCI
- 1.90
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Funders
- MEXT | Japan Society for the Promotion of Science (15H04505, 15K15104)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Vitamin C and Antioxidants Research
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Keywords
- scurvy, vitamin C, skeletal muscle atrophy, muscle atrophy, physical performance, ascorbic acid biosynthesis, ubiquitin ligase, atrogin-1, MuRF1, gastrocnemius, soleus muscle, muscle cross-sectional area, vitamin C supplementation
- MeSH terms
- Animals, Ascorbic Acid, Ascorbic Acid Deficiency, Female, Muscle Proteins, Muscular Atrophy, Up-Regulation, Mice, Knockout, Muscle, Skeletal, Ubiquitin, Ubiquitin-Protein Ligases, Mice
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