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Mothers were subjected to glucose and insulin tolerance tests at 1, 2, 3, 6, and 12 mo postweaning. Pregnant rats not treated with DEX and age-matched virgin rats were used as controls. Pancreatic islets were isolated at the 20th day of pregnancy and 12 mo postweaning in order to evaluate glucose-stimulated insulin secretion. The expression of the miR-29 family was also studied due to its responsiveness to GCs and its well-documented role in the regulation of pancreatic \u03b2-cell function. Rats treated with DEX during pregnancy presented long-term glucose intolerance and impaired insulin secretion. These changes correlated with 1) increased expression of miR-29 and its regulator p53, 2) reduced expression of syntaxin-1a, a direct target of miR-29, and 3) altered expression of genes related to cellular senescence. Our data demonstrate that the use of DEX during pregnancy results in deleterious outcomes to the maternal metabolism, hallmarked by reduced insulin secretion and glucose intolerance. This maternal metabolic programming might be a consequence of time-sustained upregulation of miR-29s in maternal pancreatic islets. <\/jats:p>","DOI":"10.1152\/ajpendo.00364.2013","type":"journal-article","created":{"date-parts":[[2013,11,20]],"date-time":"2013-11-20T00:36:46Z","timestamp":1384907806000},"page":"E109-E120","source":"Crossref","is-referenced-by-count":23,"title":["Long-term disruption of maternal glucose homeostasis induced by prenatal glucocorticoid treatment correlates with miR-29 upregulation"],"prefix":"10.1152","volume":"306","author":[{"given":"Patr\u00edcia R.","family":"Gomes","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of S\u00e3o Paulo, S\u00e3o Paulo, Brazil;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria F.","family":"Graciano","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Institute of Biomedical Sciences, 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