EFFECT OF MATERNAL FASTING ON FETAL GROWTH, SERUM INSULIN-LIKE GROWTH-FACTORS (IGFS), AND TISSUE IGF MESSENGER RIBONUCLEIC-ACIDS

Pregnant rats were fasted or allowed access to ad libitum feeds for the last 3 days of gestation to determine if the fetal growth retardation that results from maternal nutrient deprivation correlates with reductions in serum insulin-like growth factor-I (IGF-I) and IGF-II. In addition, IGF-I and IGF-II mRNA concentrations in liver and lung were measured by specific solution hybridization assays to determine if changes in steady state levels of mRNA correlate with changes in serum values. Fetal serum IGF-I concentrations were 30% lower in fasted than in control fetuses, although fasting did not significantly reduce the abundance of IGF-I mRNA in their livers or lungs. Serum IGF-I concentrations in the fasted dams were 34% lower than those in controls. IGF-I mRNA concentrations in the livers and lungs of the fasted dams were also lower than those in controls and correlated with serum IGF-I values (liver: R = 0.833; P < 0.001; lung: r = 0.610; P < 0.05). Therefore, whereas IGF-I appears to be transcriptionally regulated by fasting in dams, regulation of circulating IGF-I in fetuses may occur at a post-transcriptional step. Serum IGF-II and liver IGF-II mRNA concentrations were much higher than IGF-I levels in the fetuses and were not influenced by maternal fasting. Dam serum IGF-II concentrations were low compared to those in fetal serum and also were not reduced by fasting. We conclude that one mechanism by which maternal malnutrition causes intrauterine growth retardation is through decreased expression of IGF-I. On the other hand, short term nutrient restriction does not appear to be a regulator of IGF-II during either fetal or adult life. © 1990 by The Endocrine Society.