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

Jérôme Mairesse, Jean Lesage, Christophe Breton, Bernadette Bréant, Tom Hahn, Muriel Darnaudéry, Suzanne L. Dickson, Jonathan Seckl, Bertrand Blondeau, Didier Vieau, Stefania Maccari, Odile Viltart
American Journal of Physiology-Endocrinology and Metabolism. 2007-06-01; 292(6): E1526-E1533
DOI: 10.1152/ajpendo.00574.2006

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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 11β-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 β-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.

Auteurs Bordeaux Neurocampus