Long-term maternal-fetal exposure to high-low insulin concentrations alter liver but not brain insulin receptors.

We investigated the effects of long-term (5 to 6 days) in vivo exposure to hyperinsulinemia and hypoinsulinemia on maternal and fetal rat (18 to 20 days' gestation; term approximately 21 days) brain and liver insulin receptors. Further we studied the in vitro effects of long-term insulin exposure on cultured rabbit neuronal cell insulin receptors. Long-term glucose infusions to maternal rats resulted in maternal and fetal hyperglycemia and mild hyperinsulinemia, which decreases the liver insulin receptor abundance of the mother but increased that of the fetus. Streptozotocin-induced maternal diabetes resulted in maternal and fetal hyperglycemia with hypoinsulinemia (or near-normal insulin levels) and increased maternal and fetal liver insulin receptors. The maternal and fetal brain insulin receptor abundance failed to change at high or low insulin concentrations. Similarly long-term insulin (5 micrograms/ml) exposure failed to alter cultured neuronal cell insulin receptors as well. We conclude that perturbations in maternal and fetal circulating insulin concentrations fail to affect the brain insulin receptors. This protective phenomenon may be critical in maintaining the normal neuronal energy balance and functioning during certain disease states such as diabetes mellitus and hyperinsulinism.