Lung maturation in fetuses of diabetic rats

Abstract

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-3]choline into phosphatidylcholine and lysophospha- tidylcholine 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. Speculation: It is suggested that, in diabetic pregnancy, respiratory distress syndrome becomes manifest after a diminished availability of surface-active dipalmitic phosphatidylcholine in the fetal lung, resulting from a specific inhibition of the lysophosphatidylcholine pathway. © 1980 International Pediatric Research Foundation, Inc.