RGD Reference Report - A rodent model of low- to moderate-dose ethanol consumption during pregnancy: patterns of ethanol consumption and effects on fetal and offspring growth. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

A rodent model of low- to moderate-dose ethanol consumption during pregnancy: patterns of ethanol consumption and effects on fetal and offspring growth.

Authors: Probyn, Megan E  Zanini, Simone  Ward, Leigh C  Bertram, John F  Moritz, Karen M 
Citation: Probyn ME, etal., Reprod Fertil Dev. 2012;24(6):859-70. doi: 10.1071/RD11200.
RGD ID: 405100969
Pubmed: PMID:22781937   (View Abstract at PubMed)
DOI: DOI:10.1071/RD11200   (Journal Full-text)

It is unknown whether low to moderate maternal alcohol consumption adversely affects postnatal health. The aim of the present study was to develop a rodent model of low-moderate-dose prenatal ethanol (EtOH) exposure. Sprague-Dawley rats were fed a liquid diet with or without 6% v/v EtOH throughout gestation and the pattern of dietary consumption determined. Fetal bodyweights and hepatic alcohol-metabolising gene expression were measured on embryonic Day (E) 20 and offspring growth studied until 1 year. At E8 the plasma EtOH concentration was 0.03%. There was little difference in dietary consumption between the two treatment groups. At E20, EtOH-exposed fetuses were significantly lighter than controls and had significantly decreased ADH4 and increased CYP2E1 gene expression. Offspring killed on postnatal Day (PN) 30 did not exhibit any growth deficits. Longitudinal repeated measures of offspring growth demonstrated slower growth in males from EtOH-fed dams between 7 and 12 months of age; a cohort of male pups killed at 8 months of age had a reduced crown-rump length and kidney weight. In conclusion, a liquid diet of 6% v/v EtOH fed to pregnant dams throughout gestation caused a 3-8% reduction in fetal growth and brain sparing, with growth differences observed in male offspring later in life. This model will be useful for future studies on the effects of low-moderate EtOH on the developmental origins of health and disease.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
ADH4HumanPrenatal Exposure Delayed Effects  ISOAdh4 (Rattus norvegicus)mRNA:decreased expression:liver (rat)RGD 
Adh4RatPrenatal Exposure Delayed Effects  IEP mRNA:decreased expression:liver (rat)RGD 
Adh4MousePrenatal Exposure Delayed Effects  ISOAdh4 (Rattus norvegicus)mRNA:decreased expression:liver (rat)RGD 
CYP2E1HumanPrenatal Exposure Delayed Effects  ISOCyp2e1 (Rattus norvegicus)mRNA:increased expression:liver (rat)RGD 
Cyp2e1RatPrenatal Exposure Delayed Effects  IEP mRNA:increased expression:liver (rat)RGD 
Cyp2e1MousePrenatal Exposure Delayed Effects  ISOCyp2e1 (Rattus norvegicus)mRNA:increased expression:liver (rat)RGD 


Genes (Rattus norvegicus)
Adh4  (alcohol dehydrogenase 4 (class II), pi polypeptide) Cyp2e1  (cytochrome P450, family 2, subfamily e, polypeptide 1)

Genes (Mus musculus)
Adh4  (alcohol dehydrogenase 4 (class II), pi polypeptide) Cyp2e1  (cytochrome P450, family 2, subfamily e, polypeptide 1)

Genes (Homo sapiens)
ADH4  (alcohol dehydrogenase 4 (class II), pi polypeptide) CYP2E1  (cytochrome P450 family 2 subfamily E member 1)