The DOI matches its Crossref record; 223 of the 226 references it cites were found in a registry or an index.
Mechanisms involved in the developmental programming of adulthood disease
Abstract
There are many instances in life when the environment plays a critical role in the health outcomes of an individual, yet none more so than those experienced in fetal and neonatal life. One of the most detrimental environmental problems encountered during this critical growth period are changes in nutrition to the growing fetus and newborn. Disturbances in the supply of nutrients and oxygen to the fetus can not only lead to adverse fetal growth patterns, but they have also been associated with the development of features of metabolic syndrome in adult life. This fetal response has been termed developmental programming or the developmental origins of health and disease. The present review focuses on the epidemiological studies that identified this association and the importance that animal models have played in studying this concept. We also address the potential mechanisms that may underpin the developmental programming of future disease. It also highlights (i) how developmental plasticity, although beneficial for short-term survival, can subsequently programme glucose intolerance and insulin resistance in adult life by eliciting changes in key organ structures and the epigenome, and (ii) how aberrant mitochondrial function can potentially lead to the development of Type 2 diabetes and other features of metabolic syndrome.
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“Perturbation of gene expression or cell proliferation and differentiation during vulnerable periods by nutritional and other environmental influences can alter the structure and functional capacity of major organ systems for life, a process known as developmental programming.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [565]
In the citing paper
“The end result will be altered development of the fetal organs, as seen in cases of severe maternal undernutrition (215, 374, 565).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [565]
Citations
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Self-citation
Metadata
- Authors
- Warner, M. J., & Ozanne, S. E.
- Affiliations
- University of Cambridge (GB)
- ORCID
- Ozanne, Susan E.
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2010-04-14
- Volume
- 427
- Issue
- 3
- Pages
- 333-347
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- OpenAlex
- W1983684926
- Cited by
- 316
- References
- 226
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 18 · 2022: 14 · 2021: 13 · 2020: 23 · 2019: 14 · 2018: 13 · 2017: 15 · 2016: 27 · 2015: 30 · 2014: 21 · 2013: 39 · 2012: 37
- FWCI
- 5.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical Journal (publishedVersion)
- PubMed (publishedVersion)
- Funders
- British Heart Foundation (FS/09/029/27902)
- Biotechnology and Biological Sciences Research Council (BB/F015364/1, BB/E00797X/1)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Keywords
- developmental programming, developmental origins of health and disease, fetal nutrition, neonatal nutrition, metabolic syndrome, developmental plasticity, insulin resistance, impaired glucose tolerance, epigenome, mitochondrial dysfunction, type 2 diabetes, fetal growth restriction, animal models
- MeSH terms
- Adult, Animals, Diabetes Mellitus, Type 2, Disease Models, Animal, Female, Humans, Male, Models, Biological, Pregnancy, Prenatal Exposure Delayed Effects, Metabolic Syndrome, Prenatal Nutritional Physiological Phenomena, Fetal Development
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