Early Life Nutrition, Epigenetics and Programming of Later Life Disease
Open accessAbstract
The global pandemic of obesity and type 2 diabetes is often causally linked to marked changes in diet and lifestyle; namely marked increases in dietary intakes of high energy diets and concomitant reductions in physical activity levels. However, less attention has been paid to the role of developmental plasticity and alterations in phenotypic outcomes resulting from altered environmental conditions during the early life period. Human and experimental animal studies have highlighted the link between alterations in the early life environment and increased risk of obesity and metabolic disorders in later life. This link is conceptualised as the developmental programming hypothesis whereby environmental influences during critical periods of developmental plasticity can elicit lifelong effects on the health and well-being of the offspring. In particular, the nutritional environment in which the fetus or infant develops influences the risk of metabolic disorders in offspring. The late onset of such diseases in response to earlier transient experiences has led to the suggestion that developmental programming may have an epigenetic component, as epigenetic marks such as DNA methylation or histone tail modifications could provide a persistent memory of earlier nutritional states. Moreover, evidence exists, at least from animal models, that such epigenetic programming should be viewed as a transgenerational phenomenon. However, the mechanisms by which early environmental insults can have long-term effects on offspring are relatively unclear. Thus far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification, and microRNA) and permanent changes in cellular ageing. A better understanding of the epigenetic basis of developmental programming and how these effects may be transmitted across generations is essential for the implementation of initiatives aimed at curbing the current obesity and diabetes crisis.
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GDM exposure disrupts fetal hypothalamic development, impairing appetite regulation.
“GDM exposure disrupts fetal hypothalamic development, impairing appetite regulation.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [69]
The Animal Models section discusses hypothalamic POMC methylation in relation to neonatal leptin treatment, while the References list mentions maternal hyperglycemia in relation to IGF-1 histone modification. Neither passage says that GDM exposure disrupts fetal hypothalamic development or impairs appetite regulation. Searches for GDM, gestational diabetes, and hypothalamic appetite regulation found no passage establishing that link. (LLM, conf=0.75)
Experimental — accuracy not yet measuredCompromised development of hypothalamic circuits due to maternal hyperglycemia and impaired development and axonal growth of ARH neurons has been demonstrated.
“Recently, compromised development of hypothalamic circuits due to maternal hyperglycemia and impaired development and axonal growth of ARH neurons has been demonstrated [66,67,68,69,70].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [69]
Section 3 (Evidence from Animal Models) discusses hypothalamic POMC promoter methylation in relation to neonatal leptin treatment, not maternal hyperglycemia or impaired circuit development. Searches for ARH neurons, axonal growth, and hypothalamic projections found no passage in our copy addressing the claimed finding. (LLM, conf=0.75)
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- Authors
- Vickers, M.
- Affiliations
- University of Auckland (NZ)
- Corresponding author
- Vickers, Mark
- ORCID
- Vickers, Mark
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2014-06-02
- Volume
- 6
- Issue
- 6
- Pages
- 2165-2178
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC4073141
- OpenAlex
- W2061809258
- Cited by
- 366
- References
- 79
- Citations by year
- 2026: 17 · 2025: 15 · 2024: 18 · 2023: 13 · 2022: 28 · 2021: 23 · 2020: 39 · 2019: 46 · 2018: 41 · 2017: 41 · 2016: 43 · 2015: 29 · 2014: 13
- FWCI
- 6.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Royal Society
- Royal Society Te Apārangi
- Health Research Council of New Zealand
- Marsden Fund
- 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
- developmental programming, early life nutrition, epigenetics, obesity, type 2 diabetes, metabolic disorders, developmental plasticity, transgenerational epigenetic inheritance, DNA methylation, histone modifications, microRNA, cellular aging, critical developmental periods
- MeSH terms
- Aging, Female, Humans, Infant, Infant Nutritional Physiological Phenomena, Metabolic Diseases, Pregnancy, Maternal Nutritional Physiological Phenomena, Epigenomics
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