Phosphatidylcholine synthesis and glycogen depletion in fetal mouse lung: developmental changes and the effects of...

We measured the rate of choline incorporation into phosphatidylcholine in lung slices; the glucogen content of the lung; and the activities of pulmonary cholinephosphate cytidylyltransferase, cholinephosphotransferase and phosphatidate phosphatase in the mouse during late fetal and early postnatal development. We also examined the effect of maternal dexamethasone administration on these parameters of fetal lung maturation. There was a development increase in the rate of choline incorporation between 17 days gestation (term is 19 days) and the immediate newborn period. There was also a developmental decrease in the glycogen content of the lung but this did not occur until 18 days. There was a developmental increase in the activities of cholinephosphate cytidylytransferase and phosphatidate phosphatase but little change in the activity of cholinephosphotransferase. Dexamethasone doubled the rate of choline incorporation into phosphatidylcholine at 17 and 18 days gestation. It decreased the glycogen content of the fetal lung by 74% at 18 and 19 days, but had no effect at 16 and 17 days. Dexamethasone increased the activity of pulmonary cholinephosphate cytidylyltransferase by 37% and that of cholinephosphotransferase by 27% at 17 days. It increased the activity of phosphatidate phosphatase by 25% at 16 days and by 32% at 19 days. These data show that the normal development profile of these parameters of fetal lung maturation in the mouse, as well as the effects of glucocorticoids thereon, are generally similar to those in the rabbit and rat. However, stimulation of cholinephosphotransferase by glucocorticoids has not been generally observed in other species. Furthermore, since the changes in the rate of choline incorporation precede those in glycogen depletion, the data suggest that the relationship between phospholipid synthesis and glycogen degradation is not simply that of precursor to product.