Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome

Kaminen-Ahola, Nina, Ahola, Arttu, Flatscher-Bader, Traute, Wilkins, Sarah J., Anderson, Greg J., Whitelaw, Emma and Chong, Suyinn (2010) Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome. Birth Defects Research. Part A: Clinical and Molecular Teratology, 88 10: 818-826. doi:10.1002/bdra.20729

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Author Kaminen-Ahola, Nina
Ahola, Arttu
Flatscher-Bader, Traute
Wilkins, Sarah J.
Anderson, Greg J.
Whitelaw, Emma
Chong, Suyinn
Title Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome
Journal name Birth Defects Research. Part A: Clinical and Molecular Teratology   Check publisher's open access policy
ISSN 1542-0752
1542-0760
0040-3709
Publication date 2010-10
Sub-type Article (original research)
DOI 10.1002/bdra.20729
Volume 88
Issue 10
Start page 818
End page 826
Total pages 9
Place of publication Hoboken, NJ, U.S.A.
Publisher John Wiley & Sons
Collection year 2011
Language eng
Formatted abstract
Growth restriction, craniofacial dysmorphology, and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal or postnatal, but the underlying mechanisms remain unknown.

We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome (e.g., craniofacial changes and growth restriction in adolescent mice). In this study, we characterize in detail the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and by extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of nonfostered, ethanol-exposed and control mice at postnatal day 28.

We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This finding suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiologic result of ethanol exposure in utero. We also find that, despite some catch-up growth after 5 weeks of age, the effect extends into adulthood, which is consistent with longitudinal studies in humans.

Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis, and lipid metabolism.
© 2010 Wiley-Liss, Inc.
Keyword Fetal alcohol syndrome
Fetal alcohol spectrum disorders
Ethanol
Growth restriction
Gene expression
Mouse model
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes HERDC 2010 item added after deadline. Author/s will be asked to provide author declaration if necessary

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
Queensland Brain Institute Publications
School of Medicine Publications
 
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Created: Wed, 30 Mar 2011, 11:15:47 EST by Lisa Hennell on behalf of Queensland Brain Institute