Thyroid hormones and plasma corticosteroid binding globulin capacity in fetal and newborn lambs.
Although the increase in plasma corticosteroid binding globulin (CBG) capacity during late gestation in the fetal sheep is dependent on an intact fetal pituitary, the possible role of thyroid hormones is unknown. In rats, thyroid hormones control the postnatal increase in CBG. In the present study we investigated the effect of thyroidectomy and T3 treatment on CBG capacity in both the fetal and newborn lamb. Fifteen fetal lambs were thyroidectomized in utero at 119-121 days gestation and then infused with either vehicle or T3 (8-50 micrograms/h) for 8 days. Thyroidectomy alone did not prevent the expected increase in CBG capacity. T3 treatment of thyroidectomized fetuses caused a dose-dependent reduction in CBG capacity (maximum decrease = 31% of control). By contrast, plasma concentrations of total protein, albumin, and beta-globulins were unaltered. T3 treatment reduced plasma total corticoid concentrations, but the unbound level was unchanged. Administration of T3 (maximum dose 8 micrograms/h) to one intact fetus did not affect CBG capacity. Eleven newborn lambs were thyroidectomized between 2 and 8 days of age and infused with either vehicle or T3 (25 micrograms/h) for 8 days. Thyroidectomy alone did not prevent the normal decrease in CBG capacity after birth. T3 administration to the thyroidectomized lambs resulted in even lower plasma CBG capacity. We conclude that the prenatal increase in CBG capacity of the fetal sheep is not regulated by thyroid hormones, and that pharmacological concentrations of T3 decrease plasma CBG capacity and secondarily plasma corticoids. These findings indicate that CBG in the fetal sheep is apparently controlled by a different hormone(s) than in other species which have been studied.