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Am J Physiol Endocrinol Metab (September 26, 2006). doi:10.1152/ajpendo.00269.2006
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Submitted on June 6, 2006
Accepted on September 18, 2006

Acute ethanol exposure in pregnancy alters the insulin-like growth factor axis of fetal and maternal sheep

Kathryn L Gatford1*, Penelope A Dalitz2, Megan L Cock2, Richard Harding2, and Julie A Owens1

1 Research Centre for Reproductive Health, Discipline of Obstetrics and Gynaecology, School of Paediatrics and Reproductive Health, University of Adelaide, Adelaide, South Australia, Australia
2 Department of Physiology, Monash University, Clayton, Victoria, Australia

* To whom correspondence should be addressed. E-mail: kathy.gatford{at}adelaide.edu.au.

Maternal ethanol intake during pregnancy impairs fetal growth but mechanisms are not clearly defined. Reduced insulin-like growth factor (IGF) abundance or bioavailability in the fetus and/or mother may contribute to this growth-restriction. We hypothesised that an episode of acute ethanol exposure, mimicking "binge drinking", would restrict fetal growth and perturb the maternal and fetal IGF axes. Pregnant sheep were infused i.v. with saline or ethanol (1 g/kg maternal weight) over 1 hour, on days 116, 117 and 118 of gestation (start of 1st infusion = time 0, term is 147 days). Maternal and fetal plasma IGF and IGF-binding protein concentrations (IGFBP) were measured before and after each infusion. Compared to controls, ethanol exposure reduced fetal weight at d120 by 19%, transiently reduced maternal plasma IGF-I (-35%) at 30 h, and decreased fetal plasma IGF-II (-28%) from 24 to 54 h after the first infusion. Ethanol exposure did not alter maternal or fetal plasma concentrations of IGFBP-2 and IGFBP-3, measured by Western ligand blotting. We conclude that suppression of maternal and fetal IGF abundance may contribute to fetal growth-restriction induced by acute or "binge" ethanol exposure.




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