The pancreatic beta-cell dysfunction plays an important role on the development of type 2diabetes (DM2), and it is know that genetic and epigenetic factors contribute to thesusceptibility of this disease. Epidemiological evidences suggest that exposure to anadverse environment, in early life, is associated with an increased risk of metabolicdisorders in adulthood. Overexposure to glucocorticoids (GC), during fetal period oflife, is one important factor that impacts the development promoting glucose intolerancein adult offspring, probably by epigenetic mechanisms, which are not fully understood.Considering that genetic predisposition and environmental factors are involved with thedevelopment of DM2, and that intrauterine exposure to excess GC impairs theoffspring's pancreas function (turning them more susceptible to DM2), our objective isto assess the epigenetic mechanisms involved with this beta-cell failure. For this, we willanalyze the genone-wide DNA methylation and gene expression profile of islet fromoffspring exposed to prenatal GC. Besides that, we propose to evaluate the effect of GCon human islets and beta-cell function.
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