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Am J Physiol Endocrinol Metab 292: E1526-E1533, 2007. First published January 30, 2007; doi:10.1152/ajpendo.00574.2006
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Maternal stress alters endocrine function of the feto-placental unit in rats

Jérôme Mairesse,1,* Jean Lesage,1,* Christophe Breton,1 Bernadette Bréant,2 Tom Hahn,3 Muriel Darnaudéry,1 Suzanne L. Dickson,4 Jonathan Seckl,5 Bertrand Blondeau,2 Didier Vieau,1 Stefania Maccari,1,6 and Odile Viltart1

1Perinatal Stress Unit, University of Lille 1, Villeneuve d'Ascq; 2Institut National de la Santé et de la Recherche Médicale, Cordeliers Biomedical Research Institute, Paris, France; 3Institute of Histology and Embryology, University of Graz, Graz, Austria; 4Department Physiology/Endocrinology, Institute Neuroscience, The Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden; 5Endocrinology Unit, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom; and 6Department of Experimental Medicine and Pathology, University Rome 1 "La Sapienza", Rome, Italy

Submitted 25 October 2006 ; accepted in final form 26 January 2007

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 11beta-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.

prenatal stress; placenta; adrenal; testis; pancreas; glucose; growth hormone; adrenocorticotropic hormone


Address for reprint requests and other correspondence: S. Maccari, Perinatal Stress Unit, Bat SN4-1, Univ. of Lille 1, 59655 Villeneuve d'Ascq, France (e-mail: maccari{at}univ-lille1.fr)






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