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MicroRNA‐29 expression in pancreatic islets correlates with the impairment of maternal glucose homeostasis induced by glucocorticoid excess in late pregnancy
Author(s) -
Gomes Patricia Rodrigues Lourenço,
Graciano Maria Fernanda Rodrigues,
Pantaleão Lucas Carminati,
LellisSantos Camilo,
Carpinelli Angelo Rafael,
Latorraca Marcia Queiroz,
Bordin Silvana
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.737.2
Subject(s) - medicine , endocrinology , weaning , dexamethasone , pancreatic islets , glucose homeostasis , glucocorticoid , insulin , pregnancy , gestation , downregulation and upregulation , homeostasis , offspring , insulin resistance , biology , islet , biochemistry , gene , genetics
We investigated the long‐term effects of dexamethasone (DEX) administration during late gestation in glucose homeostasis and in the expression of miRNAs in pancreatic islets. Pregnant Wistar rats received dexamethasone (DEX), 0.2 mg/kg daily in drinking water during the last five days of pregnancy (Preg‐DEX). Age‐matched virgin female rats either treated (CTL‐DEX) or not (CTL) with DEX, as well as untreated pregnant rats (Preg) were used as controls. All groups were subjected to glucose and insulin tolerance tests at weaning and at 3, 6, and 12 month after weaning. Pancreatic islets were isolated for glucose stimulated insulin secretion (GSIS) and miRNA expression. Compared to control groups, glucose intolerance was observed in Preg‐DEX rats from weaning to 12 months after weaning. In all periods insulin sensitivity was normal. An upregulation in miR‐29 family (miR‐29a/b/c) was observed in Preg‐DEX islets at the end of gestation and 12 months after weaning. In the later period, mir‐29 expression paralleled a decrease in GSIS. In conclusion, we show that the excess of glucocorticoid in late pregnancy permanently impairs pancreatic islets function, which is correlated with persistent upregulation of miR‐29 expression. Financial support: FAPESP 2011/01568–5, PRONEX‐FAPEMAT.