ArticleEpigenetics2016
Wilson Disease: Epigenetic effects of choline supplementation on phenotype and clinical course in a mouse model.
Article in Epigenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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.
Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Choline, a nexus for neurocognitive nutrients: A narrative review.Nutrition research (New York, N.Y.) · 2026Review
- Sex-specific mitochondrial dysregulation and metformin response in Wilson disease.Scientific reports · 2026Article
- Choline and DNA methylation: impact across metabolic, oncogenic and neurodevelopmental disorders.Clinical epigenetics · 2026Review
- Mechanisms of multi-organ damage in Wilson disease from the gut-liver-brain axis perspective: copper metabolism, gut microbiota, and metabolite communication.Frontiers in microbiology · 2026Review
- Multiscale computational genomics in Wilson disease: from atomic dynamics to clinical prediction.Frontiers in genetics · 2026Review
- Nano-Mediated Molecular Targeting in Diagnosis and Mitigation of Wilson Disease.Molecular neurobiology · 2024Review
- A new Caenorhabditis elegans model to study copper toxicity in Wilson disease.Traffic (Copenhagen, Denmark) · 2024Article
- Identification of Key Genes Associated with Heat Stress in Rats by Weighted Gene Co-Expression Network Analysis.Animals : an open access journal from MDPI · 2023Article
- Article
- Correlation scan: identifying genomic regions that affect genetic correlations applied to fertility traits.BMC genomics · 2022Article
- Epigenetics in inflammatory liver diseases: A clinical perspective (Review).Experimental and therapeutic medicine · 2022Review
- Wilson Disease: Update on Pathophysiology and Treatment.Frontiers in cell and developmental biology · 2022Review
- Evaluation of the Mechanism of Jiedu Huazhuo Quyu Formula in Treating Wilson's Disease-Associated Liver Fibrosis by Network Pharmacology Analysis and Molecular Dynamics Simulation.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
- Comprehensive RNA-Seq Profiling Reveals Temporal and Tissue-Specific Changes in Gene Expression in Sprague-Dawley Rats as Response to Heat Stress Challenges.Frontiers in genetics · 2021Article
- Functional and Pathological Roles of AHCY.Frontiers in cell and developmental biology · 2021Review
- mtDNA depletion-like syndrome in Wilson disease.Liver international : official journal of the International Association for the Study of the Liver · 2020Article
- Genetics and epigenetic factors of Wilson disease.Annals of translational medicine · 2019Review
- Review
- Metabolomics profiles of patients with Wilson disease reveal a distinct metabolic signature.Metabolomics : Official journal of the Metabolomic Society · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
Wilson disease (WD), a genetic disorder affecting copper transport, is characterized by hepatic and neurological manifestations with variable and often unpredictable presentation. Global DNA methylation in liver was previously modified by dietary choline in tx-j mice, a spontaneous mutant model of WD. We therefore hypothesized that the WD phenotype and hepatic gene expression of tx-j offspring could be modified by maternal methyl supplementation during pregnancy. In an initial experiment, female tx-j mice or wild type mice were fed control or choline-supplemented diets 2 weeks prior to mating through embryonic day 17. Transcriptomic analysis (RNA-seq) on embryonic livers revealed tx-j-specific differences in genes related to oxidative phosphorylation, mitochondrial dysfunction, and the neurological disorders Huntington's disease and Alzheimer disease. Maternal choline supplementation restored the transcript levels of a subset of genes to wild type levels. In a separate experiment, a group of tx-j offspring continued to receive choline-supplemented or control diets, with or without the copper chelator penicillamine (PCA) for 12 weeks until 24 weeks of age. Combined choline supplementation and PCA treatment of 24-week-old tx-j mice was associated with increased liver transcript levels of methionine metabolism and oxidative phosphorylation-related genes. Sex differences in gene expression within each treatment group were also observed. These results demonstrate that the transcriptional changes in oxidative phosphorylation and methionine metabolism genes in WD that originate during fetal life are, in part, prevented by prenatal maternal choline supplementation, a finding with potential relevance to preventive treatments of WD.
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Registered trials
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.