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This Article Full Text Full Text (PDF) All Versions of this Article: 292/6/E1526    most recent 00574.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Mairesse, J. Articles by Viltart, O. Search for Related Content PubMed PubMed Citation Articles by Mairesse, J. Articles by Viltart, O.

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

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 11-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 -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