Lung maturation in fetuses of diabetic rats.
Pulmonary maturation in diabetic pregnancy has been studied in the 20-day-old fetuses of manifest diabetic rats. The animals were either untreated or treated with insulin. The diabetic state was induced by a single IV injection of streptozotocin given about 2 wk before the onset of pregnancy. The biosynthesis of lung surfactant was estimated by monitoring the rate of incorporation of [methyl-3H]choline into phosphatidylcholine and lysophosphatidylcholine in fetal lung slices. In the untreated group, the biosynthesis of both phosphatidylcholine and lysophosphatidylcholine were decreased in the fetal lung. Insulin treatment abolished the decrease in the phosphatidylcholine biosynthesis, whereas the lysophosphatidylcholine biosynthesis reamined depressed. Light and transmission electron microscopical studies indicated a delayed pulmonary maturation in the untreated offspring accompanied by a decreased cytoplasmic content of glycogen in the alveolar epithelial cells.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy; D005260:Female; D005325:Fetal Organ Maturity; D005333:Fetus / Q000378:metabolism; D007328:Insulin / Q000627:therapeutic use; D008168:Lung / Q000196:embryology* / Q000378:metabolism; D008244:Lysophosphatidylcholines / Q000378:metabolism; D010713:Phosphatidylcholines / Q000378:metabolism; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000188:drug therapy; D051381:Rats
D007328:Insulin; D008244:Lysophosphatidylcholines; D010713:Phosphatidylcholines