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Area of Science:

  • Developmental programming
  • Metabolic disorders
  • Endocrinology

Background:

  • Prenatal exposure to excess steroids or steroid mimics disrupts organ development.
  • The metabolic system is highly susceptible to prenatal steroid excess.
  • Such exposures can lead to adult-onset diseases.

Purpose of the Study:

  • To review cardiometabolic perturbations from prenatal steroid exposure in sheep.
  • To discuss underlying mechanisms of adverse outcomes.

Main Methods:

  • Review of studies using the sheep model.
  • Analysis of outcomes from exposure to native steroids and steroid mimics (e.g., bisphenol A).

Main Results:

  • Prenatal steroid excess causes insulin resistance, increased adiposity, altered adipocyte characteristics, and hypertension in offspring.
  • Phenotypic outcomes are similar across different prenatal insults.

Conclusions:

  • Common mechanisms like hormonal imbalances, oxidative stress, inflammation, lipotoxicity, and epigenetic alterations may underlie these effects.
  • The sheep model provides valuable mechanistic insight into prenatal programming of metabolic disease.