Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 May;29(3):225-36.
doi: 10.1055/s-0031-1275516. Epub 2011 Jun 27.

The intrauterine growth restriction phenotype: fetal adaptations and potential implications for later life insulin resistance and diabetes

Affiliations
Review

The intrauterine growth restriction phenotype: fetal adaptations and potential implications for later life insulin resistance and diabetes

Stephanie R Thorn et al. Semin Reprod Med. 2011 May.

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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Transition from insulin sensitive to insulin resistant in intrauterine growth-restricted offspring.

References

    1. Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5–20. - PubMed
    1. 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
    1. McMillen IC, Robinson JS. Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. Physiol Rev. 2005;85(2):571–633. - PubMed
    1. 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
    1. Hay WW., Jr Recent observations on the regulation of fetal metabolism by glucose. J Physiol. 2006;572(Pt 1):17–24. - PMC - PubMed