Hormonal control of lipid metabolism in mouse mammary gland explants.
Lipid biosynthesis in cultured mammary tissues from mice during midpregnancy was maximally stimulated by the combined actions of PRL, insulin, and a glucocorticoid. The minimal concentration of cortisol that was consistently permissive for the action of PRL on lipid synthesis was 0.1 microgram/ml (2.76 X 10(-7) M). The PRL effect began after 6-8 h of exposure to PRL. The response to PRL was essentially all or none, with 25 ng/ml sufficient for maximal stimulation. Specificity of the PRL effect is suggested by the observation that 1 microgram/ml bovine GH was without effect in cultured mammary tissues. Additionally, PRL had no effect on lipid metabolism in explants of ovarian fat pad, suggesting that the PRL effect in the mammary gland is not a generalized effect on fat cells. The action of PRL in the mammary gland requires both ongoing RNA and protein syntheses, since both actinomycin D and puromycin abolished its effect. The early action of PRL on lipid biosynthesis was specific for the formation of triglycerides, but not other lipid classes studied.
D000085:Acetates / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D003609:Dactinomycin / Q000494:pharmacology; D005260:Female; D005989:Glycerides / Q000096:biosynthesis; D006854:Hydrocortisone / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D008055:Lipids / Q000096:biosynthesis*; D008321:Mammary Glands, Animal / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D009924:Organ Culture Techniques; D010743:Phospholipids / Q000096:biosynthesis; D011247:Pregnancy; D011388:Prolactin / Q000494:pharmacology*; D011691:Puromycin / Q000494:pharmacology
D000085:Acetates; D005989:Glycerides; D007328:Insulin; D008055:Lipids; D010743:Phospholipids; D003609:Dactinomycin; D011691:Puromycin; D011388:Prolactin; D006854:Hydrocortisone