The DOI matches its Crossref record; 107 of the 107 references it cites were found in a registry or an index.
Impact of Maternal Diet on the Epigenome during In Utero Life and the Developmental Programming of Diseases in Childhood and Adulthood
Open accessAbstract
Exposure to environmental factors in early life can influence developmental processes and long-term health in humans. Early life nutrition and maternal diet are well-known examples of conditions shown to influence the risk of developing metabolic diseases, including type 2 diabetes mellitus and cardiovascular diseases, in adulthood. It is increasingly accepted that environmental compounds, including nutrients, can produce changes in the genome activity that, in spite of not altering the DNA sequence, can produce important, stable and, in some instances, transgenerational alterations in the phenotype. Epigenetics refers to changes in gene function that cannot be explained by changes in the DNA sequence, with DNA methylation patterns/histone modifications that can make important contributions to epigenetic memory. The epigenome can be considered as an interface between the genome and the environment that is central to the generation of phenotypes and their stability throughout the life course. To better understand the role of maternal health and nutrition in the initiation and progression of diseases in childhood and adulthood, it is necessary to identify the physiological and/or pathological roles of specific nutrients on the epigenome and how dietary interventions in utero and early life could modulate disease risk through epigenomic alteration.
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“regulation by microRNAs (miRNAs), small non-coding RNAs that post-transcriptionally regulate gene expression.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [158]
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“Together, these mechanisms form the molecular basis of fetal programming, through which maternal nutritional imbalance can imprint lasting effects on gene regulation, metabolism, and disease vulnerability in later life [157,158,159].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [158]
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“DNA methylation, mediated by DNA methyltransferases (DNMTs), which typically repress gene transcription when occurring in promoter regions;”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [158]
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“Once established early in life, these epigenetic alterations are relatively stable and may exert lifelong effects on phenotype and disease risk.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [158]
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“histone modifications (e.g., acetylation, methylation, phosphorylation) that influence chromatin structure and the accessibility of transcriptional machinery;”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [158]
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“Maternal malnutrition (whether undernutrition, overnutrition, or obesity) can induce persistent epigenetic modifications that alter gene expression without changing the DNA sequence.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [158]
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Citations
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Human–Environment Interactions: A Multi-Omics and Interactome Perspective
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Орлова, С. В., Prokopenko, E. V., Radzinsky, V. E., Никитина, Е. А., Olina, A. A., Gabidullina, R. I., Kodentsova, V. M., Risnik, D. V., & Vodolazkaya, A. N. (2025) · Medical alphabet · doi:10.33667/2078-5631-2025-19-9-13
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Metadata
- Authors
- Lee, H.-S.
- Affiliations
- Centre international de recherche sur le cancer (FR)
- Corresponding author
- Lee, Ho-Sun
- ORCID
- Lee, Ho-Sun
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2015-11-17
- Volume
- 7
- Issue
- 11
- Pages
- 9492-9507
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC4663595
- OpenAlex
- W2177368991
- Semantic Scholar
- c27867817e6f8bd06ffbdf5221390da50aadffbd
- Cited by
- 236
- References
- 107
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 12 · 2023: 20 · 2022: 25 · 2021: 19 · 2020: 23 · 2019: 32 · 2018: 33 · 2017: 23 · 2016: 16
- FWCI
- 3.64
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nutrients (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, cc-by-sa)
- Funders
- World Health Organization
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Keywords
- maternal diet, epigenetics, DNA methylation, histone modifications, developmental programming, early life nutrition, type 2 diabetes, cardiovascular disease, metabolic disorders, transgenerational epigenetic inheritance, prenatal exposure, dietary intervention
- MeSH terms
- Animals, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Diet, Disease Models, Animal, Female, Humans, Nutritional Status, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, DNA Methylation, Maternal Nutritional Physiological Phenomena, Epigenesis, Genetic, Epigenomics, Gene-Environment Interaction
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