Regulation of Fetal Lung Phosphatidyl Choline Synthesis by Cortisol: Role of Glycogen and Glucose (original) (raw)

Summary: Twenty pregnant rabbits were studied in pairs. Half were given cortisol subcutaneously on days 24. 25, and 26 of gestation in dosage of 2 nig/kg/day. Half served as controls and received saline. The fetal lungs were studied on the 27th day of gestation by incubating lung slices in the presence of [6-14C]glucose. Glucose consumption significantly increased in the tissues from animals treated with cortisol, 17.61 ± 5.56 (SD) μmol/g wet lung versus 14.28 ± 5.78 (SD) μmol/g in the controls (P < 0.05). The glycogen content of tissues treated with cortisol was significantly reduced compared to the controls, 2.42 ± 0.97 (SD) mg/g wet lung versus 3.81 ± 1.05 (SD) mg/g (P < 0.05). Treatment with cortisol resulted in significantly enhanced incorporation of the 14C label into glycogen and phosphatidl choline (Tables 3 and 4). These data suggest that glucocorticoids affect fetal lung phosphatidyl choline production by promoting glycogenolysis and increasing glucose incorporation into phosphatidyl choline.

Speculation: Diminished glycogen content of the fetal lung in the latter part of gestation may reflect increasing utilization for phosphatidyl choline synthesis. Adenosine 3′,-5′-monophosphate (cyclic AMP) increases which occur after glucocorticoid administration may be responsible for activation of glycogen phosphorylases in the lung as they are in the liver. If insulin inhibits glycogenolysis in the lung as it does in the liver, insulin may inhibit phosphatidyl choline synthesis in the lung by preventing glycogen and glucose From serving as precursors.