Intestinal function in infant rats: effect of maternal chronic ethanol ingestion

Postnatal growth retardation is one of the principle features of fetal alcohol syndrome. The cause of this growth retardation is not known. Therefore the intestinal transport of an amino acid marker, L-valine-14C, was studied in vivo in small intestinal segments of 2-week-old infant rats born to mothers fed chronically ethanol during pregnancy. Control infant rats were born to mothers isocalorically pair fed throughout pregnancy. Transport rates of L-valine expressed on the basis of unit weight or unit length were similar in both groups of rats. We concluded that this neutral amino acid transport pathway was unaltered in infants of mothers fed chronic ethanol during pregnancy. Thus, the growth retardation seen in fetal alcohol syndrome is unlikely to be secondary to intestinal protein malabsorption.