ArticleScientific reports2020
Ascorbic acid during the suckling period is required for proper DNA demethylation in the liver.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Physicochemical properties and differential metabolites associated with mustard fermentation by Pediococcus pentosaceus and Lactiplantibacillus pentosus compound.BMC microbiology · 2025Article
- Exploring the Ascorbate Requirement of the 2-Oxoglutarate-Dependent Dioxygenases.Journal of medicinal chemistry · 2025Review
- Effects of Low Vitamin C Intake on Fertility Parameters and Pregnancy Outcomes in Guinea Pigs.Nutrients · 2023Article
- PPARα in the Epigenetic Driver Seat of NAFLD: New Therapeutic Opportunities for Epigenetic Drugs?Biomedicines · 2022Review
- TargetingCancers · 2022Review
- Ascorbate Is a Primary Antioxidant in Mammals.Molecules (Basel, Switzerland) · 2022Review
- The Epigenetic Role of Vitamin C in Neurodevelopment.International journal of molecular sciences · 2022Review
- The PPARα and PPARγ Epigenetic Landscape in Cancer and Immune and Metabolic Disorders.International journal of molecular sciences · 2021Review
- Review
- Microbial Cell Factories for Green Production of Vitamins.Frontiers in bioengineering and biotechnology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ascorbic acid (AA, vitamin C) serves as a cofactor for ten-eleven translocation (TET) enzymes and induces DNA demethylation in vitro. However, its role in DNA demethylation in vivo remains unclear. We previously reported that DNA demethylation in the mouse liver was enhanced during the suckling period. Therefore, we hypothesized that DNA demethylation is enhanced in an AA-dependent manner during the suckling period. To examine our hypothesis, we employed wild-type (WT) mice, which synthesize AA, and senescence marker protein-30/gluconolactonase (SMP30/GNL) knockout (KO) mice, which cannot synthesize AA, and analyzed the DNA methylation status in the livers of offspring in both the suckling period and adulthood. SMP30/GNL KO offspring showed DNA hypermethylation in the liver possibly due to low plasma and hepatic AA levels during the suckling period despite the administration of rescue-dose AA to dams. Furthermore, DNA hypermethylation of the fibroblast growth factor 21 gene (Fgf21), a PPARα target gene, persisted into adulthood. In contrast, a high-dose AA administration to SMP30/GNL KO dams during the lactation period restored DNA demethylation in the livers of offspring. Even though a slight increase was observed in plasma AA levels with the administration of rescue-dose AA to WT dams during the gestation and lactation periods, DNA demethylation in the livers of offspring was minimally enhanced. The present results demonstrate that AA intake during the suckling period is required for proper DNA demethylation in the liver.
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