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Gomes PRL. Efeito da exposição à dexametasona sobre a expressão de miRNA no pâncreas endócrino e a homeostasia glicêmica de ratas prenhes. [PhD Thesis (Human Physiology)]. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo; 2014. Several studies have focused on the metabolic programming in pregnancy induced glucocorticoid excess, with special attention to the mechanisms that lead to the onset of various diseases and even genetic reprogramming in offspring. However, the impact by glucocorticoid excess during pregnancy on the maternal metabolism is not well documented. Therefore, this study investigated whether treatment with synthetic glucocorticoids during pregnancy alters the energetic, hormonal and molecular maternal metabolism and function of pancreatic islets and correlative changes of miRNAs and their targets. For this were used 80 rats divided into two groups of 40 animals each, one group designed to perform GTT, ITT and aging up to one year of age after weaning, and the next group destined to collect the materials and later experimentation the 20 th day of gestation. Both groups were arranged: CTL control rats, CTL-Dex control rats treated with dexamethasone for 6 days, P pregnant rats and PDex pregnant rats treated with dexamethasone from the 14 th to 19 th day of gestation. The pancreatic islets were collected for large-scale analysis of miRNA expression and the miR29 ́s family was selected for further study. The target genes were screened in databases and confirmed by real-time PCR. Finally it was investigated the mechanism of modulation of glucose homeostasis through real-time PCR and Western Blotting. The profile of miR-29 observed in P-Dex group immediately after treatment remained one year after weaning of the offspring. Analysis of mRNA from the same tissue showed significant modulation of p53, PUMA and Stx-1genes in P-Dex group both on day 20 of gestation as one year after weaning of the offspring. In addition to these changes was observed glucose intolerance in P-Dex group at weaning, at 3 rd and 6 th months and one year after weaning of offspring, however, resistance to insulin was not observed in the same periods. Insulin secretion of islets collected on the 20 th day of gestation showed no changes. On the other hand, one year after weaning was observed that the P-Dex group responded to the test at high glucose concentrations. Finally, were observed significant changes in progesterone receptor and proteins involved in the remodeling of pancreatic islets responsible for returning at non pregnant state. Therefore can be observed numerous changes resulting from therapy with DEXA in pregnancy concluded that the association of treatment to the pregnancy period modulates members of the miRNA-29 family causing an imbalance in glucose homeostasis through long-term failure in exocytotic machinery, triggered by the downregulation of the progesterone and its receptor promoting injury in the pancreatic islet remodeling process in late pregnancy.