Periconceptional alcohol consumption causes fetal growth restriction and increases glycogen accumulation in the late gestation rat placenta

Gardebjer E.M., Cuffe J.S.M., Pantaleon M., Wlodek M.E. and Moritz K.M. (2014) Periconceptional alcohol consumption causes fetal growth restriction and increases glycogen accumulation in the late gestation rat placenta. Placenta, 35 1: 50-57. doi:10.1016/j.placenta.2013.10.008


Author Gardebjer E.M.
Cuffe J.S.M.
Pantaleon M.
Wlodek M.E.
Moritz K.M.
Title Periconceptional alcohol consumption causes fetal growth restriction and increases glycogen accumulation in the late gestation rat placenta
Journal name Placenta   Check publisher's open access policy
ISSN 0143-4004
1532-3102
Publication date 2014-01-01
Year available 2013
Sub-type Article (original research)
DOI 10.1016/j.placenta.2013.10.008
Volume 35
Issue 1
Start page 50
End page 57
Total pages 8
Place of publication London, United Kingdom
Publisher Elsevier
Language eng
Formatted abstract
Introduction:
Alcohol consumption is a common social practice among women of childbearing age. With 50% of pregnancies being unplanned, many embryos are exposed to alcohol prior to pregnancy recognition and formation of the placenta. The effects of periconceptional (PC) alcohol exposure on the placenta are unknown.

Methods:
Sprague-Dawley rats were exposed to alcohol (12.5% v/v ad libitum) from 4 days prior to 4 days after conception and effects on placental growth, morphology and gene/protein expression examined at embryonic day (E) 20.

Results:
PC ethanol (EtOH)-exposed fetuses were growth restricted and their placental/body weight ratio and placental cross-sectional area were increased. This was associated with an increase in cross-sectional area of the junctional zone and glycogen cells, especially in PC EtOH-exposed placentas from female fetuses. Junctional Glut1 and Igf2 mRNA levels were increased. Labyrinth Igf1 mRNA levels were decreased in placentas from both sexes, but protein IGF1R levels were decreased in placentas from male fetuses only. Labyrinth mRNA levels of Slc38a2 were decreased and Vegfa were increased in placentas following PC EtOH-exposure but only placentas from female fetuses exhibited increased Kdr expression. Augmented expression of the protective enzyme 11βHsd2 was found in PC EtOH-exposed labyrinth.

Discussion:
These observations are consistent with a stress response, apparent well beyond the period of EtOH-exposure and demonstrate that PC EtOH alters placental development in a sex specific manner.

Conclusion:
Public awareness should be increased to educate women about how excessive drinking even before falling pregnant may impact on placental development and fetal health.
Keyword Ethanol
Glycogen
Periconceptional
Placenta
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Biomedical Sciences Publications
 
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