TISSUE AND SERUM CONCENTRATIONS OF SOMATOMEDIN-C INSULIN-LIKE GROWTH FACTOR-I IN FETAL RATS MADE GROWTH RETARDED BY UTERINE ARTERY LIGATION

To study the role of somatomedin-C/insulin-like growth factor I (Sm-C/IGF I) in fetal growth, intrauterine growth retardation was induced by uterine artery ligation on day 17 of gestation in pregnant rats. Fetuses of the nonligated horns served as appropriately grown controls. On day 21 of gestation, fetal serum, liver, and lung were obtained and analyzed for Sm-C/IGF I by radioimmunoassay. Serum insulin was determined by radioimmunoassay and serum glucose by a glucose oxidase method. Fetal weight, serum concentrations of glucose, insulin and Sm-C/IGF I, and liver Sm-C/IGF I concentrations were reduced in fetuses from uterine artery ligated horns as compared to those from nonligated control horns. Fetal weight was correlated with serum glucose (r = 0.703; p < 0.001), liver Sm-C/IGF I (r = 0.682; p < 0.001), and serum Sm-C/IGF I (r = 0.452; p < 0.001). Stepwise linear regression demonstrated that these three factors in combination correlated highly with fetal weight (r = 0.836). No correlation was found for serum insulin or lung Sm-C/IGF I and fetal weight. Serum insulin concentrations correlated with serum, but not liver, Sm-C/IGF I concentrations, making a direct effect of insulin on Sm-C/IGF I synthesis appear unlikely. However, serum glucose concentrations correlated with liver (r = 0.404; p < 0.001) and with serum Sm-C/IGF I (r = 0.308; p < 0.002) concentrations, implicating fetal glucose delivery in the regulation of Sm-C/IGF I synthesis. Taken together, these data suggest that Sm-C/IGF I synthesis in the fetus is influenced by nutrition and that Sm-C/IGF I plays a mediating role in the control of growth.