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Cell Press, Cell Metabolism, 1(8), p. 5-7, 2008

DOI: 10.1016/j.cmet.2008.06.007

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Diabetes Risk Begins In Utero

Journal article published in 2008 by Melissa Woo, Mary-Elizabeth Patti ORCID
This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

Full text: Unavailable

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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.