Maternal stress alters endocrine function of the feto-placental unit in rats

Jerome Mairesse, Jean Lesage, Christophe Breton, Bernadette Breant, Tom Hahn, Muriel Darnaudery, Suzanne L. Dickson, Jonathan Seckl, Bertrand Blondeau, Didier Vieau, Stefania Maccari, Odile Viltart

Research output: Contribution to journalArticlepeer-review


Prenatal stress ( PS) can cause early and long- term developmental effects resulting in part from altered maternal and/ or fetal glucocorticoid exposure. The aim of the present study was to assess the impact of chronic restraint stress during late gestation on feto- placental unit physiology and function in embryonic ( E) day 21 male rat fetuses. Chronic stress decreased body weight gain and food intake of the dams and increased their adrenal weight. In the placenta of PS rats, the expression of glucose transporter type 1 ( GLUT1) was decreased, whereas GLUT3 and GLUT4 were slightly increased. Moreover, placental expression and activity of the glucocorticoid " barrier" enzyme 11 beta-hydroxysteroid dehydrogenase type 2 was strongly reduced. At E21, PS fetuses exhibited decreased body, adrenal pancreas, and testis weights. These alterations were associated with reduced pancreatic beta-cell mass, plasma levels of glucose, growth hormone, and ACTH, whereas corticosterone, insulin, IGF-1, and CBG levels were unaffected. These data emphasize the impact of PS on both fetal growth and endocrine function as well as on placental physiology, suggesting that PS could program processes implied in adult biology and pathophysiology.

Original languageEnglish
Pages (from-to)E1526-E1533
Number of pages8
JournalAJP - Endocrinology and Metabolism
Issue number6
Publication statusPublished - Jun 2007

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