Journal Article A Complex Noncoordinate Regulation of α-Lactalbumin and 25 K β-Casein by Corticosterone, Prolactin, and Insulin in Long Term Cultures of Normal Rat Mammary Cells Get access DURWOOD B. RAY, DURWOOD B. RAY 1Departments of Medicine, Case Western Reserve University Cleveland, Ohio 44106; Departments of Biochemistry, Case Western Reserve University Cleveland, Ohio 44106; The Veterans Administration Medical Center Cleveland, Ohio 44106 Search for other works by this author on: Oxford Academic Google Scholar ROBERT W. JANSEN, ROBERT W. JANSEN 1Departments of Medicine, Case Western Reserve University Cleveland, Ohio 44106; Departments of Biochemistry, Case Western Reserve University Cleveland, Ohio 44106; The Veterans Administration Medical Center Cleveland, Ohio 44106 Search for other works by this author on: Oxford Academic Google Scholar IRIS A. HORST, IRIS A. HORST 1Departments of Medicine, Case Western Reserve University Cleveland, Ohio 44106; Departments of Biochemistry, Case Western Reserve University Cleveland, Ohio 44106; The Veterans Administration Medical Center Cleveland, Ohio 44106 Search for other works by this author on: Oxford Academic Google Scholar NATHANIEL C. MILLS, NATHANIEL C. MILLS 1Departments of Medicine, Case Western Reserve University Cleveland, Ohio 44106; Departments of Biochemistry, Case Western Reserve University Cleveland, Ohio 44106; The Veterans Administration Medical Center Cleveland, Ohio 44106 Search for other works by this author on: Oxford Academic Google Scholar JEROME KOWAL JEROME KOWAL 1Departments of Medicine, Case Western Reserve University Cleveland, Ohio 44106; Departments of Biochemistry, Case Western Reserve University Cleveland, Ohio 44106; The Veterans Administration Medical Center Cleveland, Ohio 44106 Search for other works by this author on: Oxford Academic Google Scholar Endocrinology, Volume 118, Issue 1, 1 January 1986, Pages 393–407, https://doi.org/10.1210/endo-118-1-393 Published: 01 January 1986 Article history Received: 09 April 1984 Published: 01 January 1986
Article1 July 1963"Pituitary Reserve" in Myxedema and ThyrotoxicosisJEROME KOWAL, M.D., LOUIS J. SOFFER, M.D., F.A.C.P.JEROME KOWAL, M.D.Search for more papers by this author, LOUIS J. SOFFER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-59-1-79 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe effects of abnormal thyroid function on the elaboration and metabolism of carbon-19 and carbon-21 steroids have been well described (1-3). In hyperthyroidism, the metabolic degradation of these compounds is increased, the adrenal cortex compensating for this by an increased elaboration of these compounds. That this increased turnover may result in a limited pituitary or adrenal reserve in these patients is suggested by the efficacy of corticosteroids in the treatment of thyroid "storm" (4). However, Sagan, Perloff, and DiRaimondo (5) found a normal adrenal response to a single 8-hour intravenous infusion of adrenocorticotropic hormone (ACTH). Other investigators have confirmed this...References1. PETERSON RE: The miscible pool and turnover rate of adrenocortical steroids in man. Rec. Prog. Hormone Res. 15: 231, 1959. Google Scholar2. BROWNENGLERTWALLACH HES: Metabolism of free and conjugated 17-hydroxycorticosteroids in subjects with thyroid disease. J. Clin. Endocr. 18: 167, 1958. CrossrefMedlineGoogle Scholar3. LEVINDAUGHADAY EWH: The influence of the thyroid in adrenocortical function. J. Clin. Endocr. 15: 1499, 1955. CrossrefGoogle Scholar4. GOLDKENTFORSHAM EMJRPH: Clinical use of a new diagnostic agent, methopyrapone (SU-4885), in pituitary and adrenocortical disorders. Ann. Intern. Med. 54: 175, 1961. LinkGoogle Scholar5. SAGANPERLOFFDIRAIMONDO LPVC: Studies of the fate of adrenal corticoids in hyper and hypothyroidism. Abstract 101, presented at the thirty-ninth meeting of the Endocrine Society, New York, 1957. Google Scholar6. FELBERREDDYSELENKOWTHORN JPWJHAGW: Adrenocortical response to the 48-hour ACTH test in myxedema and hyperthyroidism. J. Clin. Endocr. 19: 895, 1959. CrossrefGoogle Scholar7. MIKULAJNEMETH LS: Letter to the editor. J. Clin. Endocr. 18: 539, 1958. CrossrefGoogle Scholar8. HILLFORSHAMROCHETHORN SRPHMGW: The response of the adrenal cortex and thyroid gland to ACTH and cortisone in patients with hypothyroidism and the nephrotic syndrome. J. Clin. Endocr. 10: 1375, 1950. CrossrefGoogle Scholar9. STATLANDLERMAN HJ: Function of the adrenal cortex in myxedema, with some observations on pituitary function. Ibid., 1401. Google Scholar10. ZARROWZARROW MXIG Mechanism of adrenal involution in the rat after treatment with thiouracil. Proc. Soc. Exp. Biol. Med. 76: 620, 1951. CrossrefMedlineGoogle Scholar11. MICHIELTRON-LOISELTRUCHOT RHR: Influence de l'activité thyroidienne sur la sécrétion de la corticotrophine hypophysaire et de la chlorpromazine sur celle de la thyréostimuline. C. R. Soc. Biol. (Paris) 153: 569: 1959. Google Scholar12. KOWALEWSKI K: Effect of corticotrophin on the plasma 17-hydroxycorticoids in normal thiouracil treated guinea pigs. Acta Endocr. 27: 257, 1958. MedlineGoogle Scholar13. LIDDLEESTEPKENDALLWILLIAMSTOWNES GWHLJWWCAW: Clinical application of a new test of pituitary reserve. J. Clin. Endocr. 19: 875, 1959. CrossrefMedlineGoogle Scholar14. BISSELLSCOTTFARNSWORTHWINKLER GWALWEI: A preliminary study of the use of 2-methyl-1,2-bis (3-pyridil)-1-propanone (SU-4885) as a test of pituitary function in man. New York J. Med. 59: 3596, 1959. MedlineGoogle Scholar15. BROWNIESPRUNT ACJC: Metopirone in the assessment of pituitary-adrenal function. Lancet 1: 773, 1962. CrossrefMedlineGoogle Scholar16. SILBERPORTER RHCC: The determination of 17,21-dihydroxy-20-ketosteroids in urine and plasma. J. Biol. Chem. 210: 923, 1954. CrossrefMedlineGoogle Scholar17. PETERSONKARRERGUERRA REASL: Evaluation of Silber-Porter procedure for determination of plasma hydrocortisone. Anal. Chem. 29: 144, 1957. CrossrefGoogle Scholar18. DREKTERHEISLERSCISMSTERNPearsonMCGAVACK IJAGRSETH: The preparation of pigment-free extracts and a simplified procedure for the estimation of total 17-ketosteroids. J. Clin. Endocr. 12: 55, 1952. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, New YorkFrom the Endocrine Research Laboratory of the Department of Medicine, The Mount Sinai Hospital, New York, New York.At the time of this study, Dr. Kowal was a Trainee of the National Institutes of Health, United States Public Health Service.Requests for reprints should be addressed to Jerome Kowal, M.D., The Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByHypothalmic-pituitary-adrenal function in thyroid disorders: Effects of methopyrapone infusion on plasma corticosteroids 1 July 1963Volume 59, Issue 1_Part_1Page: 79-83KeywordsAdrenocorticotropic hormoneExcretionHospital medicineHyperthyroidismMedical servicesPrevention, policy, and public healthResearch laboratoriesSteroidsStormsThyroid Issue Published: 1 July 1963 PDF DownloadLoading ...
Following 15-30 min exposure to monensin, adrenocorticotropic hormone (ACTH)- stimulated steroidogenesis in cultured adrenal cells is inhibited by 37-48 %. Electron microscopic studies reveal that, in monensin-treated cells, the Golgi complexes are disrupted into large vacuolar structures with loss of its organized structure indicating that the action of monensin on the organelles is comparably rapid. The inhibition is fully reversed after removal of the monensin-containing medium and exposure to fresh growth medium for a subsequent 4-24 h prior to stimulation. Concomitant with the restoration of full steroidogenic activity, the disrupted organelles are extensively reorganized in the cells after exposure to fresh growth medium for 4-24 h. These findings, which demonstrate, for the first time, a correlation between the morphology of the Golgi complex and steroidogenic activity, strengthen the possibility that the organelle may be involved in the regulation of steroidogenesis.
Vasoactive intestinal peptide (VIP) has been shown to be steroidogenic in monolayer cultures of a murine adrenal tumor but must be present at concentrations about 100-fold greater than ACTH to elicit the same degree of stimulation. Both peptides enhanced cAMP synthesis, although there was again a difference of 2 orders of magnitude in the dose-response curves. In contrast, VIP stimulated adenyl cyclase activity of tumor membranes in the same concentration range as ACTH. Maximum activity with VIP was less than that with ACTH in the absence or presence of a saturating amount of guanylyl imido-diphosphate. Saturating amounts of both peptides stimulated activity to levels greater than that with either ACTH or VIP alone, but the activity was not fully additive. An o-nitrophenyl sulfenyl derivative of ACTH inhibited ACTH-stimulated adenyl cyclase activity but not VIP-stimulated activity. Low concentrations of calcium potentiated the ability of submaximal doses of ACTH to stimulate adenyl cyclase but had no effect on the response to VIP. Concentrations of secretin or glucagon comparable to that of VIP did not stimulate steroidogenesis in intact cells. These data suggest that VIP may bind to a unique receptor which may be distinct from that of ACTH.
