Lactogenic receptor regulation in hormone-stimulated steroidogenic cells

• Published in: Nature (London) 1980-02, Vol.283 (5750), p.863-865
• Main Authors: Davies, Terry F, Katikineni, Mohan, Chan, Vivian, Harwood, James P, Dufau, Maria L, Catt, Kevin J
• Format: Article
• Language: English
• Subjects: Adrenal Glands - metabolism; Adrenocorticotropic Hormone - pharmacology; Animals; Chorionic Gonadotropin - metabolism; Chorionic Gonadotropin - pharmacology; Female; Growth Hormone - metabolism; Humanities and Social Sciences; letter; Male; multidisciplinary; Ovary - metabolism; Rats; Receptor, Insulin - metabolism; Receptors, Cell Surface - drug effects; Receptors, Cell Surface - metabolism; Receptors, Cell Surface - physiology; Science; Science (multidisciplinary); Steroids - biosynthesis; Testis - metabolism
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/283863a0

Receptor sites for lactogenic hormones such as prolactin (PRL), human growth hormone (HGH), and placental lactogens, are widely distributed in mammalian tissues, including mammary glands 1 , steroid-secreting cells of the adrenal, testis, and ovary, and target cells of steroid hormone action such as liver, prostrate, and kidney 2,3 . Although the biological functions of lactogen binding sites remain uncertain, a relationship between prolactin and lipoprotein metabolism is implied by the occurrence of prolactin receptors in steroidogenic cells of the gonads and adrenal, and by the ability of prolactin to increase esterified cholesterol in the testis 4 . Recently, loss of testicular prolactin receptors has been observed following elevation of circulating luteinising hormone (LH) concentrations by the gonadotropin releasing hormone (GnRH) and its agonist analogues 5,6 . The hormone dependence of lactogen receptor sites in steroid-secreting cells was further analysed in rat testis, ovary, and adrenal glands after treatment with the respective trophic hormones, gonadotropin and ACTH. In each of these tissues, rapid and transient loss of lactogen receptors was observed after trophic hormone stimulation. These findings indicate that increased turnover of lactogen receptors is an important component of the target-cell response, and suggest that prolactin receptors might be involved in the transport of lipoprotein precursors for steroid biosynthesis.