Abstract
The infant of the diabetic mother shows delayed lung maturation and available evidence suggests that both hyperinsulinemia and hyperglycemia may mediate this delay. In vitro studies have shown that insulin blocks cortisol stimulation of surfactant-associated phospholipid synthesis. Cortisol induces the synthesis of fibroblast-pneumonocyte factor (FPF) which in turn stimulates surfactant synthesis by alveolar type II cells. In the present study, we have examined the effects of insulin, cortisol and FPF on saturated phosphatidylcholine (SPC) synthesis by fetal type II cells alone and in the presence of fetal lung fibroblasts and the effects of insulin and cortisol upon the production of FPF activity by fetal lung fibroblasts. In fibroblast/type II cell cultures, cortisol stimulates (3H)choline incorporation into SPC and this effect is blocked by insulin as well as by monoclonal antibodies directed against FPF. In type II cell cultures, cortisol is ineffective but SPC synthesis is stimulated by FPF. This stimulation is not inhibited by insulin. In contrast, preliminary studies suggest that insulin inhibits the elaboration of FPF activity by fetal lung fibroblasts exposed to cortisol.
These observations confirm the ability of insulin to block cortisol induction of lung maturation and suggest that this action is exerted on the fetal lung mesenchyme.
(Supported by NIH grant HL-25907)
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Carlson, K., Post, M. & Smith, B. THE CELLULAR SITE OF INSULIN INHIBITION OF GLUCOCORTICOID-INDUCED LUNG MATURATION. Pediatr Res 18 (Suppl 4), 388 (1984). https://doi.org/10.1203/00006450-198404001-01770
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DOI: https://doi.org/10.1203/00006450-198404001-01770
