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

Journal article
Authors 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
Published in American journal of physiology. Endocrinology and metabolism
Volume 292
Issue 6
Pages E1526-33
ISSN 0193-1849
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages E1526-33
Language en
Keywords 11-beta-Hydroxysteroid Dehydrogenase Type 2, metabolism, Adrenal Glands, pathology, Animals, Blood Glucose, metabolism, Body Weight, Chronic Disease, Eating, Endocrine Glands, embryology, Female, Fetal Blood, metabolism, Fetus, anatomy & histology, metabolism, Glucose Transport Proteins, Facilitative, metabolism, Hormones, blood, Insulin-Secreting Cells, cytology, Islets of Langerhans, embryology, Male, Organ Size, Pancreas, embryology, Placenta, metabolism, Pregnancy, Pregnancy Complications, metabolism, pathology, physiopathology, Rats, Restraint, Physical, Stress, etiology, metabolism, pathology, physiopathology, Testis, embryology
Subject categories Physiology, Neurophysiology, Nutrition and Dietetics


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.

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