TY - JOUR
T1 - Glucocorticoids, hyperinsulinemia, and fetal lung maturation
AU - Beck, J. C.
AU - Johnson, J. W.C.
AU - Mitzner, W.
AU - Lee, Peter
AU - London, W. T.
AU - Sly, D. L.
N1 - Funding Information:
This study was supported in part by National Institutes of Health Research Grant No. HD-04050. Dr. Mitzner received National Institutes of Health Research Career Development Award No. HL-00347.
PY - 1981
Y1 - 1981
N2 - 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.
AB - 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.
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U2 - 10.1016/0002-9378(81)90326-4
DO - 10.1016/0002-9378(81)90326-4
M3 - Article
C2 - 7008612
AN - SCOPUS:0019379079
VL - 139
SP - 465
EP - 470
JO - [No source information available]
JF - [No source information available]
SN - 0042-1215
IS - 4
ER -