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


CONCLUSIONS
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.


CONCLUSIONS
Public awareness should be increased to educate women about how excessive drinking even before falling pregnant may impact on placental development and fetal health.
School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland 4072, Australia.
E M
EM
Gårdebjer
School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland 4072, Australia.
J S M
JS
Cuffe
School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland 4072, Australia.
M
M
Pantaleon
The Department of Physiology, The University of Melbourne, Parkville, Victoria 3010, Australia.
M E
ME
Wlodek
School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland 4072, Australia. Electronic address: k.moritz@uq.edu.au.
K M
KM
Moritz
D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D047108:Embryonic Development; D000431:Ethanol / Q000009:adverse effects* / Q000097:blood; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000209:etiology*; D006003:Glycogen / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D010920:Placenta / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors
D000431:Ethanol; D007334:Insulin-Like Growth Factor I; D006003:Glycogen
Ethanol; Glycogen; Periconceptional; Placenta; Preimplantation