Cited by 153Birth, Development, and HealthPregnancy and preeclampsia studiesGestational Diabetes Research and Management

The Intrauterine Growth Restriction Phenotype: Fetal Adaptations and Potential Implications for Later Life Insulin Resistance and Diabetes

Open access
Thorn, Stephanie, Rozance, Paul, Brown, Laura, Hay, William·2011·Seminars in Reproductive Medicine

Abstract

The intrauterine growth restricted (IUGR) fetus develops unique metabolic adaptations in response to exposure to reduced nutrient supply. These adaptations provide survival value for the fetus by enhancing the capacity of the fetus to take up and use nutrients, thereby reducing the need for nutrient supply. Each organ and tissue in the fetus adapts differently, with the brain showing the greatest capacity for maintaining nutrient supply and growth. Such adaptations, if persistent, also have the potential in later life to promote nutrient uptake and storage, which directly lead to complications of obesity, insulin resistance, reduced insulin production, and type 2 diabetes.

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Crossref · 10.1055/s-0031-1275516

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  • Maternal undernutrition may lead to foetal growth restriction, characterised by reduced pancreatic growth, impaired insulin secretion, and hepatic insulin resistance.

    “Maternal undernutrition may lead to foetal growth restriction (FGR), characterised by reduced pancreatic growth, impaired insulin secretion, and hepatic insulin resistance [28,29,30].”

    From Medical Nutrition Therapy for Women with Gestational Diabetes: Current Practice and Future Perspectives (2025) · cites this paper as [29]

    The fetal muscle-growth section describes maternal nutrient restriction in sheep models of IUGR, and the reduced pancreatic β-cell mass and insulin production section reports smaller pancreatic islets, reduced pancreas weight, and impaired insulin secretion in growth-restricted fetuses. The increased hepatic glucose production section says the IUGR fetal liver *may be developing* insulin resistance and calls for further studies of fetal hepatic insulin sensitivity. The claim presents hepatic insulin resistance as an established characteristic rather than a possibility. (LLM, conf=0.86)

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Research works printed but not linked: 2

  1. [60]Inskip HM Godfrey KM Martin HJ Simmonds SJ Cooper C Sayer AA Southampton Women’s Survey Study Group Size at birth and its relation to muscle strength in young adult women J Intern Med 2007 262 3 368 374 17697158 PMC2062503
  2. [109]Desai M Byrne CD Zhang J Petry CJ Lucas A Hales CN Programming of hepatic insulin-sensitive enzymes in offspring of rat dams fed a protein-restricted diet Am J Physiol 1997 272 5 Pt 1 G1083 G1090 9176217

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Authors
Thorn, S., Rozance, P., Brown, L., & Hay, W.
Affiliations
University of Colorado Anschutz (US)
Venue
Seminars in Reproductive Medicine
Published
2011-05
Volume
29
Issue
03
Pages
225-236
ISSN
  • 1526-4564 (ISSN-L)
  • 1526-8004
OpenAlex
W2059299661
Cited by
153
References
122
Citations by year
2026: 9 · 2025: 11 · 2024: 10 · 2023: 4 · 2022: 12 · 2021: 10 · 2020: 16 · 2019: 17 · 2018: 8 · 2017: 7 · 2016: 13 · 2015: 14 · 2014: 7 · 2013: 9 · 2012: 5
FWCI
6.52
Type
journal article
Language
en
Open access
Locations
  • Seminars in Reproductive Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases (K01DK090199)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD057022, K08HD060688)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
fetal growth restriction, fetal brain, insulin resistance, type 2 diabetes, obesity, developmental origins of health and disease, fetal programming, insulin production
MeSH terms
Adaptation, Physiological, Adult, Animals, Diabetes Mellitus, Type 2, Female, Fetal Growth Retardation, Humans, Insulin Resistance, Male, Obesity, Pregnancy, Prenatal Exposure Delayed Effects, Fetal Development

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