Tl. Buchmiller-crair et al., Delayed disaccharidase development in a rabbit model of intrauterine growth retardation, PEDIAT RES, 50(4), 2001, pp. 520-524
Intrauterine growth retardation (IUGR) affects almost 10% of I infants born
in the United States. It may be responsible for delayed gastrointestinal f
unction and is an important cause of perinatal morbidity and mortality. The
New Zealand White rabbit provides an optimal model for the study of natura
lly occurring IUGR. At term, birth weight is determined by fetal position w
ithin the bicornuate uterus. The small intestinal disaccharidase enzymes ar
e indicators of bowel maturity and function. To examine potential differenc
es in disaccharidase, development between normal and IUGR fetuses, this rab
bit model was investigated. Jejunum was harvested at multiple stages in rab
bit development including the third trimester fetus, neonate, and adult. La
ctase, maltase, and sucrase enzyme activity, as well as total protein conte
nt, was determined. Results were analyzed by 2-tailed t test and ANOVA. Lac
tase, activity appeared in the mid-third trimester, peaked in the early neo
natal period, then declined to adult levels. Maltase activity appeared in t
he early third trimester and gradually rose to adult levels. Sucrase remain
ed at trace levels until the mid-neonatal period, reaching adult levels by
weaning. Both lactase and maltase activity were depressed in IUGR fetuses c
ompared with their normal littermates. This pattern of disaccharidase depre
ssion continued into the neonatal period until catch-up growth occurred at
2 wk when levels equalized. This report describes differential small intest
inal disaccharidase development between normal and growth-retarded rabbit f
etuses in a naturally occurring model of IUGR.