Cell Press, Cell Metabolism, 1(8), p. 5-7, 2008
DOI: 10.1016/j.cmet.2008.06.007
Full text: Unavailable
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.