Diabetes risk begins in utero

Cell Metab. 2008 Jul;8(1):5-7. doi: 10.1016/j.cmet.2008.06.007.


Both intrauterine and postnatal environments contribute to diabetes risk. A recent paper highlights epigenetic mechanisms underlying beta cell dysfunction associated with intrauterine growth retardation, including repressive histone modification and DNA methylation during postnatal life. Thus, intrauterine stress can initiate a disturbing epigenetic cascade of progressive transcriptional repression linked to beta cell failure.

Publication types

  • Review

MeSH terms

  • Diabetes Mellitus / etiology*
  • Disease Susceptibility
  • Epigenesis, Genetic
  • Female
  • Fetal Growth Retardation
  • Fetus
  • Humans
  • Nutritional Status
  • Obesity
  • Pregnancy
  • Risk Factors