RGD Reference Report - Periconceptional alcohol consumption causes fetal growth restriction and increases glycogen accumulation in the late gestation rat placenta. - Rat Genome Database

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

Authors: Gårdebjer, E M  Cuffe, J S M  Pantaleon, M  Wlodek, M E  Moritz, K M 
Citation: Gårdebjer EM, etal., Placenta. 2014 Jan;35(1):50-7. doi: 10.1016/j.placenta.2013.10.008. Epub 2013 Nov 5.
RGD ID: 12904720
Pubmed: PMID:24239160   (View Abstract at PubMed)
DOI: DOI:10.1016/j.placenta.2013.10.008   (Journal Full-text)


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 11ßHsd2 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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Fetal Growth Retardation onsetISOIgf1 (Rattus norvegicus)12904720; 12904720protein:decreased expression:placenta labyrinth (rat)RGD 
Fetal Growth Retardation onsetISOIgf1r (Rattus norvegicus)12904720; 12904720protein:decreased expression:placenta labyrinth (rat)RGD 
Fetal Growth Retardation onsetIEP 12904720; 12904720protein:decreased expression:placenta labyrinth (rat)RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to ethanol  IEP 12904720; 12904720 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Igf1  (insulin-like growth factor 1)
Igf1r  (insulin-like growth factor 1 receptor)

Genes (Mus musculus)
Igf1  (insulin-like growth factor 1)
Igf1r  (insulin-like growth factor I receptor)

Genes (Homo sapiens)
IGF1  (insulin like growth factor 1)
IGF1R  (insulin like growth factor 1 receptor)


Additional Information