501 SOMATOMEDIN (Sm-C) in FETAL GROWTH

In the postnatal rat, suboptimal nutrition leads to a decrease in Sm-C which may account for the resultant decrease in growth. To study the effect of fetal malnutrition on serum and tissue Sm-C concentrations, intrauterine growth retardation(IUGR) was induced by uterine artery ligation on day 17 of gestation in 15 pregnant rats. Fetuses of the non-ligated horns served as appropriately grown(AGA) controls. After surgery the animals were allowed ad libitum feeding. On day 21 fetal blood and organs were obtained and analyzed for Sm-C and insulin by radioimmunoassay and glucose by glucose oxidase. Data are presented in relation to uterine position with 1 denoting the fetus nearest the ovarian artery. At each position, IUGR fetuses had decreased weight, serum and liver Sm-C, glucose, and insulin concentrations. (x±sem, *p<.05) Fetal weight was significantly related to glucose (r=.730), liver Sm-C (r=.682) and serum Sm-C (r=.452). Stepwise linear regression demonstrated that these three factors in combination correlated highly with fetal weight (r=.836). A weaker correlation existed for insulin (r=.378) and lung Sm-C (r=.209). These data indicate that, in the fetus, Sm-C is influenced by nutrition and may have a mediating role in the control of growth.