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  • Title: Reversal of lung maturational delay in the fetus of the diabetic rat using triiodothyronine or dexamethasone.
    Author: Rotenberg M, Gewolb IH.
    Journal: Biol Neonate; 1993; 64(5):318-24. PubMed ID: 8297942.
    Abstract:
    Administration of glucocorticoids and thyroid hormone can accelerate fetal lung development. To investigate whether the delayed fetal lung maturation seen in the diabetic rat gestation could be reversed by dexamethasone (DEX) or triiodothyronine (T3), 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 T3 until sacrifice on day 21 or day 22. While DEX did not change glucose levels in diabetic animals, T3 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 < 0.05) serum glucose concentrations. DEX therapy exaggerated the reduction in body and lung weight seen in fetuses of streptozotocin-diabetic dams. Fetal lung phosphatidylcholine and disaturated phosphatidylcholine levels were significantly reduced in saline-treated diabetic animals as compared with controls. However, fetuses of T3- or DEX-treated diabetic rats had significantly increased lung phosphatidylcholine and disaturated phosphatidylcholine levels were significantly reduced in saline-treated diabetic animals as compared with controls. However, fetuses of T3- or DEX-treated diabetic rats had significantly increased lung phosphatidylcholine and disaturated phosphatidylcholine levels as compared with fetuses of untreated diabetic rats; these data suggest that maternal DEX or T3 therapy reverses the delayed fetal lung maturation seen in the diabetic rat gestation. Since glucocorticoids can exacerbate maternal diabetes, treatment with thyroid hormone may be more appropriate, although risks must be weighed against potential benefits.
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