Glucocorticoids, hyperinsulinemia, and fetal lung maturation.
Glucocorticoids are reported to accelerate fetal lung development, whereas insulin is alleged to interfere with this effect of glucocorticoids. A paradox exists, however, in that glucocorticoids also induce hyperinsulinemia. The purpose of this study was to explore the interrelationships of betamethasone, hyperinsulinemia, and hyperglycemia to fetal lung maturation. In this rhesus preparation, maternal betamethasone administration produced an alarming increase in maternal and fetal plasma insulin values. A significant increase in total lung volumes also occurred, but lung surfactant properties (as measured by amniotic fluid lecithin/sphingomyelin concentrations, lung alveolar deflation stability, and lung phosphatidylcholine concentrations) remained unchanged. These findings are consistent with the following hypotheses: (1) Betamethasone-induced hyperinsulinemia impairs acceleration of surfactant production but does not negate increases in maximum lung volume; (2) betamethasone-induced increases in maximum lung volume occur through mechanisms other than alveolar surfactant alterations.
D000653:Amniotic Fluid / Q000032:analysis; D000818:Animals; D001623:Betamethasone / Q000494:pharmacology*; D005260:Female; D005312:Fetal Blood / Q000032:analysis; D005325:Fetal Organ Maturity / Q000187:drug effects*; D005947:Glucose / Q000032:analysis; D007328:Insulin / Q000032:analysis*; D008168:Lung / Q000033:anatomy & histology / Q000187:drug effects*; D008253:Macaca mulatta; D008297:Male; D010713:Phosphatidylcholines / Q000032:analysis; D011247:Pregnancy; D011650:Pulmonary Alveoli / Q000187:drug effects; D013109:Sphingomyelins / Q000032:analysis
D007328:Insulin; D010713:Phosphatidylcholines; D013109:Sphingomyelins; D001623:Betamethasone; D005947:Glucose