The effects of maternal diabetes upon fetal lung surfactant phospholipid metabolism were studied using 19-day gestational age fetal rats from mothers with streptozotocin-induced diabetes mellitus. In this experimental animal model, maternal glucose intolerance significantly impaired fetal body and lung development. However, incorporation of [14C]palmitate and [3H]choline into lung total and disaturated phosphatidylcholine was unimpaired in offspring of diabetic mothers. Dexamethasone, which is known to promote fetal lung maturation in normal pregnancies, was administered to diabetic and control mothers during late gestation. Prenatal dexamethasone inhibited lung growth in both diabetic and control pregnancies. While this agent slightly stimulated [14C]palmitate incorporation into total phosphatidylcholine and markedly enhanced [3H]choline incorporation into both disaturated and total phosphatidylcholine in control pregnancies, it failed to stimulate incorporation of either precursor into fetal lung from diabetic pregnancies.
|Original language||English (US)|
|Number of pages||8|
|Journal||Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism|
|State||Published - Apr 23 1981|
Bibliographical noteFunding Information:
The authors wish to thank Barbara Jensen, Melissa West, Lisa Wincentsen and Laura Classen for their expert technical assistance. This study was supported in part by grants to M.Y.T. from the Juvenile Diabetes Foundation (79R139), the Minnesota Medical Foundation (DRF-3-78), the American Diabetes Association, Minnesota Affiliate, and the Graduate School of the University of Minnesota.
Copyright 2014 Elsevier B.V., All rights reserved.
- (Fetal lung)
- Dexamethasone treatment
- Maternal diabetes
- Phosphatidylcholine synthesis