Regulation of fetal lung phosphatidyl choline synthesis by cortisol: role of glycogen and glucose.
Twenty pregnant rabbits were studied in pairs. Half were given cortisol subcutaneously on days 24, 25, and 26 of gestation in dosage of 2 mg/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 tissue from animals treated with cortisol, 17.61 "/- 5.56 (SD) mumol/g in the controls (P less than 0.05). The glycogen content of tissue 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 less than 0.05). Treatment with cortisol resulted in significantly enhanced incorporation of the 14C label into glycogen and phosphatidyl 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.
D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism*; D006854:Hydrocortisone / Q000008:administration & dosage / Q000494:pharmacology*; D050356:Lipid Metabolism; D008168:Lung / Q000378:metabolism*; D010713:Phosphatidylcholines / Q000096:biosynthesis*; D010714:Phosphatidylethanolamines / Q000378:metabolism; D011247:Pregnancy; D011817:Rabbits
D010713:Phosphatidylcholines; D010714:Phosphatidylethanolamines; D002245:Carbon Dioxide; D006003:Glycogen; D005947:Glucose; D006854:Hydrocortisone