Buts J P, Sokal E M, Van Hoof F
Laboratory of Pediatric Gastroenterology, Faculty of Medicine, University of Louvain, Brussels, Belgium.
Pediatr Res. 1992 Nov;32(5):574-9. doi: 10.1203/00006450-199211000-00018.
To examine the effects of prenatal exposure to ethanol on postnatal development of small intestinal and liver functions, female rats were accustomed to increasing amounts of ethanol (10 to 25%, vol/vol) in tap water for 1 mo. During pregnancy, ethanol-fed dams had higher daily caloric intake and similar weight gain compared with controls. In ethanol offspring, neonatal mortality was 28.9% compared to 0% in controls. Although ethanol had been withdrawn at birth, pups issued from ethanol-treated mothers showed at 5 and 10 d postpartum decreased values of body weight, jejunal and ileal weights, and intestinal DNA concentration per unit of length, as well as lower specific and total activities in lactase and maltase, compared with controls. DNA synthesis rates, measured by the incorporation of [3H]thymidine into mucosal DNA, were also significantly (-20 to -34%, p < 0.01) depressed in the jejunum and ileum of ethanol pups at 5 and 10 d of age. All these parameters returned to control levels by d 15 postpartum. Electron microscopy of jejunal mucosal samples at 5, 10, and 15 d of age revealed that ethanol pups differed from controls by a fetal-like immature aspect of the enterocytes, which persisted up to d 15. The ontogenic upsurge in sucrase and the decline in lactase occurred at weaning with the same chronology in both groups, but the level reached by sucrase activity was about 50% lower in alcohol offspring than in controls. Except for moderate steatosis, the ultrastructure of hepatocytes was unaltered in sucklings.(ABSTRACT TRUNCATED AT 250 WORDS)
