Role of prolactin, cortisol, and insulin in the regulation of surfactant synthesis by the human fetal lung.
Cortisol, in combination with prolactin and/or insulin, increases the rate of lamellar body phosphatidylcholine synthesis and markedly increases the secretion of lamellar bodies into the ductular lumens of human fetal lung explants maintained in serum-free medium. This combination also alters glycerophospholipids of lamellar bodies formed in the explants to resemble surfactant secreted by the human fetal lung at term. The suggested inhibitory effect of insulin on surfactant synthesis by the fetal lung was not supported by this study.
D002794:Choline / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D005994:Glycerophosphates / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D008055:Lipids / Q000032:analysis; D008168:Lung / Q000196:embryology / Q000378:metabolism*; D009924:Organ Culture Techniques; D010713:Phosphatidylcholines / Q000096:biosynthesis*; D010758:Phosphorus / Q000032:analysis; D011388:Prolactin / Q000494:pharmacology*; D011650:Pulmonary Alveoli / Q000032:analysis / Q000648:ultrastructure
D005994:Glycerophosphates; D007328:Insulin; D008055:Lipids; D010713:Phosphatidylcholines; D010758:Phosphorus; D011388:Prolactin; D002794:Choline; D005990:Glycerol; D006854:Hydrocortisone