Insulin-like growth factor I in substrate-deprived, growth-retarded fetal rats

Plasma, amniotic fluid, and tissue concentrations of IGF-I were examined in nutritionally deprived, growth-retarded fetal rats to determine whether IGF-I concentration serves as a marker for nutritional status. Growth retardation was induced by 72 h of maternal fasting. Twenty-three control and 17 growth-retarded fetuses were individually analyzed and compared. Plasma IGF-I concentrations were significantly lower in test compared with control animals (test 56.8 +/- 14.9, control 87.4 +/- 17.5 ng/mL, p less than 0.01). Amniotic fluid IGF-I concentrations were not different (test 14.0 +/- 8.7, control 12.2 +/- 2.6 ng/mL). IGF-I concentrations obtained from both placental and hepatic tissues were lower in test compared with control animals [placenta: test 293 +/- 25 versus control 655 +/- 114 ng/g (p less than 0.001); hepatic: test 173 +/- 38 versus control 230 +/- 51 ng/g (p less than 0.01)]. Reductions in fetal, placental, and hepatic weights in test animals were more closely related to changes in placental IGF-I concentration than to either plasma or hepatic IGF-I concentrations. We conclude that fetal plasma IGF-I is a valuable marker for intrauterine substrate deprivation and that the growth-retarded rat fetus is accurately identified and specifically characterized by a low placental concentration of extractable IGF-I.