Abstract
Respiratory distress syndrome (RDS) is due to a deficiency of dipalmitoyl lecithin (DPL), the developmental appearance of which is controlled in the fetal lung by glucocorticoid (GC) induction of choline phos-photransferase (CPT). GC produce their effects by binding to cytosolic receptors which in turn bind to nuclei and induce DNA-transcription and consequently enzyme synthesis. Since infants of diabetic mothers (IDM) have an increased incidence of RDS, we investigated this relationship by producing hyperglycemic rats with streptozotocin (STZ), prior to implantation. Mothers were consistently hyperglycemic (> 250mg%). One day prior to term, fetuses were obtained. The concentration of fetal lung cytosol dexamethasone receptor at saturating concentration (2×10-8M) was unchanged (500.4 vs. 515.8 fmole/mg prot.). However, in vitro DNA-cellulose affinity and CPT activity were decreased in the fetuses of treated animals (128.6 vs. 236.0 f.mole/mg prot. and 1.28 vs. 4.24 p.mole/min./mg, protein respectively; p < 0.05 for both). It is concluded that the fetus of the STZ-treated hyperglycemic rat is a useful model for RDS in the IDM, and suggests that steroid receptor DNA-affinity may affect DPL production and the incidence of RDS.
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Boutwell, W., Decrea, A. 172 DECREASED DNA-CELLULOSE AFFINITY OF LUNG GLUCOCORTICOID RECEPTORS IN THE FETUS OF HYPERCLYCEMIC RATS. Pediatr Res 12 (Suppl 4), 392 (1978). https://doi.org/10.1203/00006450-197804001-00177
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DOI: https://doi.org/10.1203/00006450-197804001-00177