Fetal programming: causes and consequences as revealed by studies of dietary manipulation in rats - a review

H J McArdle, H S Andersen, H Jones, L Gambling

Research output: Contribution to journalArticlepeer-review

68 Citations (Scopus)

Abstract

During pregnancy, the developing fetus is dependent on its mother for all nutritional requirements. It is not Surprising, therefore, that variations in maternal nutrition can be reflected in alterations in fetal health and well-being. Interestingly, the changes can persist into adulthood and may result in increased risk of diseases such as diabetes, obesity and cardiovascular disease. The first observations of these phenomena resulted in the development of hypotheses collectively brought under the heading of "fetal" or, more recently, "developmental" programming. In this review, we will examine some of the animal models used to understand the mechanisms involved and attempt to determine whether there are common, "gatekeeper", pathways or genes, altered by the different nutritional stresses. We will concentrate primarily on nutrition related to post-natal development of hypertension and will restrict the review to studies in rodents, since that is where most of the mechanistic studies are being undertaken. Our conclusions are that, while there may well be some common gatekeeper pathways, there is also some diversity of mechanism which may contribute to the generation of the same or similar phenotypes.

Original languageEnglish
Pages (from-to)S56-S60
Number of pages5
JournalPlacenta
Volume27
Issue numberSupplement A
Early online date13 Mar 2006
DOIs
Publication statusPublished - Apr 2006
Event11th Meeting of the European Placenta Group - Glasgow, United Kingdom
Duration: 3 Sept 20057 Sept 2005

Keywords

  • fetal programming
  • iron metabolism
  • predictive adaptive responses
  • low protein diet
  • maternal iron restriction
  • blood pressure
  • pregnant rats
  • birth weight
  • 11-beta-hydroxysteroid dehydrogenases
  • glucocorticoid exposure
  • developmental origins
  • vascular dysfunction
  • adult hypertension

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