Diabetes risk begins in utero.
review · Level V
Where this comes from
- Record sourced from PubMed, PMID 18590686.
- Also identified by DOI 10.1016/j.cmet.2008.06.007.
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Abstract
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.
Medical subject headings
- Diabetes Mellitus