Evidence map›Paper›PMID 30894591›Full record

ArticleScientific reports2019

Vitamin C deficiency causes muscle atrophy and a deterioration in physical performance.

Shoko Takisawa, Tomoko Funakoshi, Tomofumi Yatsu, Kisaburo Nagata, Toshiro Aigaki, Shuichi Machida, Akihito Ishigami

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Shoko TakisawaMolecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.
Tomoko FunakoshiMolecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.
Tomofumi YatsuMolecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.ORCID 0000-0002-7205-8573
Kisaburo NagataDepartment of Biomolecular Science, Faculty of Science, Toho University, Chiba, 274-8510, Japan.
Toshiro AigakiCellular Genetics, Graduate School of Science and Engineering, Tokyo Metropolitan University, Tokyo, 192-0397, Japan.
Shuichi MachidaGraduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan.
Akihito IshigamiMolecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan. ishigami@tmig.or.jp.ORCID 0000-0001-7875-7482
Tokyo Metropolitan Institute of Gerontology · JPToho University · JPJuntendo University · JPTokyo Metropolitan University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsAscorbic AcidAscorbic Acid DeficiencyFemaleMiceMice, KnockoutMuscle ProteinsMuscle, SkeletalMuscular AtrophyUbiquitinUbiquitin-Protein LigasesUp-RegulationAscorbic AcidMuscle ProteinsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID30894591
PMCPMC6426981
OpenAlexW2923144925

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.