title: Maternal stress alters endocrine function of the feto-placental unit in rats.
abstract: 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.
authors.affiliation: Perinatal Stress Unit, Bat SN4-1, Univ. of Lille 1, 59655 Villeneuve d'Ascq, France.
authors.forename: Jérôme
authors.initials: J
authors.lastname: Mairesse
authors.forename: Jean
authors.initials: J
authors.lastname: Lesage
authors.forename: Christophe
authors.initials: C
authors.lastname: Breton
authors.forename: Bernadette
authors.initials: B
authors.lastname: Bréant
authors.forename: Tom
authors.initials: T
authors.lastname: Hahn
authors.forename: Muriel
authors.initials: M
authors.lastname: Darnaudéry
authors.forename: Suzanne L
authors.initials: SL
authors.lastname: Dickson
authors.forename: Jonathan
authors.initials: J
authors.lastname: Seckl
authors.forename: Bertrand
authors.initials: B
authors.lastname: Blondeau
authors.forename: Didier
authors.initials: D
authors.lastname: Vieau
authors.forename: Stefania
authors.initials: S
authors.lastname: Maccari
authors.forename: Odile
authors.initials: O
authors.lastname: Viltart
mesh_terms: D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism; D000311:Adrenal Glands / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002908:Chronic Disease; D004435:Eating; D004702:Endocrine Glands / Q000196:embryology*; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005333:Fetus / Q000033:anatomy & histology / Q000378:metabolism; D051246:Glucose Transport Proteins, Facilitative / Q000378:metabolism; D006728:Hormones / Q000097:blood; D050417:Insulin-Secreting Cells / Q000166:cytology; D007515:Islets of Langerhans / Q000196:embryology; D008297:Male; D009929:Organ Size; D010179:Pancreas / Q000196:embryology; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000209:etiology / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013737:Testis / Q000196:embryology
chemical_list: D001786:Blood Glucose; D051246:Glucose Transport Proteins, Facilitative; D006728:Hormones; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2