Diabetes risk begins in utero.
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.
Woo
Melissa
M
Research Division, Joslin Diabetes Center, 1 Joslin Place, Boston, MA 02215, USA.
Patti
Mary-Elizabeth
ME
D003920:Diabetes Mellitus / Q000209:etiology*; D004198:Disease Susceptibility; D044127:Epigenesis, Genetic; D005260:Female; D005317:Fetal Growth Retardation; D005333:Fetus; D006801:Humans; D009752:Nutritional Status; D009765:Obesity; D011247:Pregnancy; D012307:Risk Factors