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Division of Pediatric Gastroenterology-Nutrition and VA Medical Center, and Department of Pediatrics, Vanderbilt Medical School, Nashville, TN 37232
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.
KEY WORDS: fetal alcohol syndrome L-valine transport infant rats
1 This study was supported in part by Biomedical Research Grant No. 523748 and the Thrasher Foundation.
2 To whom reprint requests should be sent: Department of Pediatrics, Vanderbilt Medical School, Nashville, TN 37232.
Manuscript received 5 January 1981.