REVERSAL OF LUNG MATURATIONAL DELAY IN THE FETUS OF THE DIABETIC RAT USING TRIIODOTHYRONINE OR DEXAMETHASONE

Administration of glucocorticoids and thyroid hormone can accelerate f etal lung development. To investigate whether the delayed fetal lung m aturation seen in the diabetic rat gestation could be reversed by dexa methasone (DEX) or triiodothyronine (T-3), control and streptozotocin- diabetic dams were injected daily from day 18 of gestation with either saline, 0.5 mg/kg DEX, or 1 mg/kg T-3 until sacrifice on day 21 or da y 22. While DEX did not change glucose levels in diabetic animals, T-3 resulted in a slight reduction in both maternal (474 +/- 25 vs. 539 /- 17 mg%; p < 0.07) and fetal (354 +/- 43 vs. 404 +/- 26 mg%; p < 0.0 5) serum glucose concentrations. DEX therapy exaggerated the reduction in body and lung weight seen in fetuses of streptozotocin-diabetic da ms. Fetal lung phosphatidylcholine and disaturated phosphatidylcholine levels were significantly reduced in saline-treated diabetic animals as compared with controls. However, fetuses of T-3- or DEX-treated dia betic rats had significantly increased lung phosphatidylcholine and di saturated phosphatidylcholine levels as compared with fetuses of untre ated diabetic rats; these data suggest that maternal DEX or T-3 therap y reverses the delayed fetal lung maturation seen in the diabetic rat gestation. Since glucocorticoids can exacerbate maternal diabetes, tre atment with thyroid hormone may be more appropriate, although risks mu st be weighed against potential benefits.