Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Nat Rev Endocrinol. 2009 Nov;5(11):604-10. doi: 10.1038/nrendo.2009.195. Epub 2009 Sep 29.

Nutritional programming of the metabolic syndrome.

Author information

  • 1Early Life Nutrition Research Unit, Academic Child Health, Division of Human Development, School of Clinical Sciences, University Hospital, Nottingham, UK. michael.symonds@nottingham.ac.uk

Abstract

The primary markers of the metabolic syndrome are central obesity, insulin resistance and hypertension. In this review, we consider the effect of changes in maternal nutrition during critical windows in fetal development on an individual's subsequent predisposition to the metabolic syndrome. The fetal origins of obesity, cardiovascular disease and insulin resistance have been investigated in a wide range of epidemiological and animal studies; these investigations highlight adaptations made by the nutritionally manipulated fetus that aim to maintain energy homeostasis to ensure survival. One consequence of such developmental plasticity may be a long term re-setting of cellular energy homeostasis, most probably via epigenetic modification of genes involved in a number of key regulatory pathways. For example, reduced maternal-fetal nutrition during early gestation to midgestation affects adipose tissue development and adiposity of the fetus by setting an increased number of adipocyte precursor cells. Importantly, clinically relevant adaptations to nutritional challenges in utero may only manifest as primary components of the metabolic syndrome if followed by a period of accelerated growth early in the postnatal period and/or if offspring become obese.

PMID:
19786987
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Write to the Help Desk