Cited by 158Birth, Development, and HealthEpigenetics and DNA MethylationGenetic Syndromes and Imprinting

Epigenetic Programming and Fetal Metabolic Programming

Open access
Zhu, Ziqiang, Cao, Fang, Li, Xiaozhong·2019·Frontiers in Endocrinology

Abstract

Fetal metabolic programming caused by the adverse intrauterine environment can induce metabolic syndrome in adult offspring. Adverse intrauterine environment introduces fetal long-term relatively irreversible changes in organs and metabolism, and thus causes fetal metabolic programming leading metabolic syndrome in adult offspring. Fetal metabolic programming of obesity and insulin resistance plays a key role in this process. The mechanism of fetal metabolic programming is still not very clear. It is suggested that epigenetic programming, also induced by the adverse intrauterine environment, is a critical underlying mechanism of fetal metabolic programming. Fetal epigenetic programming affects gene expression changes and cellular function through epigenetic modifications without DNA nucleotide sequence changes. Epigenetic modifications can be relatively stably retained and transmitted through mitosis and generations, and thereby induce the development of metabolic syndrome in adult offspring. This manuscript provides an overview of the critical role of epigenetic programming in fetal metabolic programming.

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Crossref · 10.3389/fendo.2019.00764

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  • Such changes may also modify placental nutrient transport, promote compensatory nutrient delivery, and predispose offspring to metabolic disorders later in life.

    “Such changes may also modify placental nutrient transport, promote compensatory nutrient delivery and predispose offspring to metabolic disorders later in life [18,173,174].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [18]

    The Fetal Metabolic Programming section says adverse intrauterine conditions may lead to obesity, insulin resistance, and metabolic syndrome in adult offspring. The cited paper discusses placental methylation in the Epigenetic Programming of Obesity section, but the passages found do not establish modified placental nutrient transport or compensatory nutrient delivery (searched: nutrient transport, placental transport, compensatory). (LLM, conf=0.86)

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2 retracted

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Authors
Zhu, Z., Cao, F., & Li, X.
Affiliations
  • Soochow University (CN)
  • Nanjing Medical University (CN)
Corresponding author
Li, Xiaozhong
Venue
Frontiers in Endocrinology
Published
2019-12-03
Volume
10
Pages
764-764
ISSN
1664-2392 (ISSN-L)
OpenAlex
W2981958174
Cited by
158
References
199
Citations by year
2026: 27 · 2025: 24 · 2024: 24 · 2023: 23 · 2022: 21 · 2021: 22 · 2020: 17
FWCI
3.16
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Endocrinology (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
Jiangsu Commission of Health
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 › Genetic Syndromes and Imprinting
Keywords
epigenetic programming, metabolic syndrome, adult offspring, obesity, insulin resistance, epigenetic modifications, transgenerational epigenetic inheritance, fetal development

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