The intrauterine growth restriction phenotype: fetal adaptations and potential implications for later life insulin resistance and diabetes
- PMID: 21710398
- PMCID: PMC3216466
- DOI: 10.1055/s-0031-1275516
The intrauterine growth restriction phenotype: fetal adaptations and potential implications for later life insulin resistance and diabetes
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.
© Thieme Medical Publishers.
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References
-
- Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5–20. - PubMed
-
- Simmons RA. Developmental origins of beta-cell failure in type 2 diabetes: the role of epigenetic mechanisms. Pediatr Res. 2007;61(5 Pt 2):64R–67R. - PubMed
-
- McMillen IC, Robinson JS. Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. Physiol Rev. 2005;85(2):571–633. - PubMed
-
- Gluckman PD, Hanson MA, Buklijas T, Low FM, Beedle AS. Epigenetic mechanisms that underpin metabolic and cardiovascular diseases. Nat Rev Endocrinol. 2009;5(7):401–408. - PubMed