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Ethanol-induced inhibition of fetal hypothalamic–pituitary–adrenal axis due to prenatal overexposure to maternal glucocorticoid in mice

Prenatal ethanol exposure has been well documented to be one of the etiological factors responsible for intrauterine growth retardation (IUGR). Previous studies have shown that chronic ethanol exposure during pregnancy elevated the basic level of corticosterone in fetus. However, the potential mecha... Full description

Journal Title: Experimental and Toxicologic Pathology 2011, Vol.63(7), pp.607-611
Main Author: Liang, Gai
Other Authors: Chen, Man , Pan, Xiao-Liang , Zheng, Jiang , Wang, Hui
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0940-2993 ; E-ISSN: 1618-1433 ; DOI: 10.1016/j.etp.2010.04.015
Link: https://www.sciencedirect.com/science/article/pii/S0940299310000783
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recordid: elsevier_sdoi_10_1016_j_etp_2010_04_015
title: Ethanol-induced inhibition of fetal hypothalamic–pituitary–adrenal axis due to prenatal overexposure to maternal glucocorticoid in mice
format: Article
creator:
  • Liang, Gai
  • Chen, Man
  • Pan, Xiao-Liang
  • Zheng, Jiang
  • Wang, Hui
subjects:
  • Prenatal Ethanol Exposure
  • Intrauterine Growth Retardation
  • Corticosterone 11β-Hydroxysteroid Dehydrogenase Type 2
  • Hypothalamus–Pituitary–Adrenal
  • Steroidogenic Acute Regulatory Protein
  • P450scc
  • Medicine
ispartof: Experimental and Toxicologic Pathology, 2011, Vol.63(7), pp.607-611
description: Prenatal ethanol exposure has been well documented to be one of the etiological factors responsible for intrauterine growth retardation (IUGR). Previous studies have shown that chronic ethanol exposure during pregnancy elevated the basic level of corticosterone in fetus. However, the potential mechanisms behind them are still unclear. The aim of the present study was to investigate the effects of prenatal ethanol exposure on maternal and fetal hypothalamic–pituitary–adrenal (HPA) axis as well as placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), and to clarify the mechanism of ethanol-induced IUGR. Pregnant mice were intragastricly administrated with ethanol at a dose of 6.4 g kg d from day 11 to 17 of gestation and parameters representing fetal growth and development were recorded either. The level of corticosterone in maternal serum was determined...
language: eng
source:
identifier: ISSN: 0940-2993 ; E-ISSN: 1618-1433 ; DOI: 10.1016/j.etp.2010.04.015
fulltext: fulltext
issn:
  • 0940-2993
  • 09402993
  • 1618-1433
  • 16181433
url: Link


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titleEthanol-induced inhibition of fetal hypothalamic–pituitary–adrenal axis due to prenatal overexposure to maternal glucocorticoid in mice
creatorLiang, Gai ; Chen, Man ; Pan, Xiao-Liang ; Zheng, Jiang ; Wang, Hui
ispartofExperimental and Toxicologic Pathology, 2011, Vol.63(7), pp.607-611
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subjectPrenatal Ethanol Exposure ; Intrauterine Growth Retardation ; Corticosterone 11β-Hydroxysteroid Dehydrogenase Type 2 ; Hypothalamus–Pituitary–Adrenal ; Steroidogenic Acute Regulatory Protein ; P450scc ; Medicine
descriptionPrenatal ethanol exposure has been well documented to be one of the etiological factors responsible for intrauterine growth retardation (IUGR). Previous studies have shown that chronic ethanol exposure during pregnancy elevated the basic level of corticosterone in fetus. However, the potential mechanisms behind them are still unclear. The aim of the present study was to investigate the effects of prenatal ethanol exposure on maternal and fetal hypothalamic–pituitary–adrenal (HPA) axis as well as placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), and to clarify the mechanism of ethanol-induced IUGR. Pregnant mice were intragastricly administrated with ethanol at a dose of 6.4 g kg d from day 11 to 17 of gestation and parameters representing fetal growth and development were recorded either. The level of corticosterone in maternal serum was determined...
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