This work was supported by Grant AA06611 (1–7) from the National Institute on Alcohol Abuse and Alcoholism.
Perinatal Maternal Ethanol Effects on Pregnant Mice and on Offspring Viability and Growth: Influences of Exposure Time and Weaning Diet
Article first published online: 11 APR 2006
DOI: 10.1111/j.1530-0277.1995.tb01624.x
Issue
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Alcoholism: Clinical and Experimental Research
Volume 19, Issue 5, pages 1351–1358, October 1995
Additional Information
How to Cite
Middaugh, L. D. and Boggan, W. O. (1995), Perinatal Maternal Ethanol Effects on Pregnant Mice and on Offspring Viability and Growth: Influences of Exposure Time and Weaning Diet. Alcoholism: Clinical and Experimental Research, 19: 1351–1358. doi: 10.1111/j.1530-0277.1995.tb01624.x
Publication History
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication July 19, 1994; accepted May 17, 1995
- Abstract
- References
- Cited By
Keywords:
- Fetal Ethanol;
- Prenatal and Postnatal Growth;
- C57BL/6 Mice
C57BL/6 mice were maintained on liquid diets containing 27.5% ethanol-derived calories beginning on gestational day 12. For one group, the liquid diet was replaced with laboratory chow on the morning of gestational day 18, ±24 hr before delivery. For a second group, the diet was continued for 7 days postnatally. Two additional groups were pair-fed isocaloric sucrose diets, and a final group was maintained on normal laboratory chow. The mice consumed sufficient amounts of diet to provide near 30 g ethanol/kg/day during pregnancy and slightly greater amounts during the first postpartum week. The ethanol diet produced no maternal deaths and did not alter weight gain during gestational days 12–17 of pregnancy. The results confirmed previous reports that dietary ethanol exposure under conditions that have rather minor effects on the pregnant mouse can substantially affect the fetus. As previously reported, when exposure was terminated 24 hr before delivery, neonatal mortality was elevated by -30%, but birth weight was not altered. When the diet was extended into the lactation period, mortality was delayed but not reduced, possibly by reducing the severity of ethanol withdrawal. Birthweight was reduced by 10% when exposure continued until birth, suggesting that low birthweights for fetal ethanol-exposed (FEE) mice can be eliminated by terminating exposure –24 hr before delivery. As in previous reports, FEE mice with normal birthweights had an attenuated preadolescent growth spurt, suggesting that low birthweights and attenuated postnatal growth are likely mediated by different mechanisms. The reduction in periadolescent growth of FEE mice resulted in weight deficits that persisted into adulthood and could not be accounted for by a reduction in calories consumed.

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