This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by HANING, R. V. Articles by LONGCOPE, C. Search for Related Content PubMed PubMed Citation Articles by HANING, R. V., Jr. Articles by LONGCOPE, C.

Metabolism of Dehydroepiandrosterone Sulfate (DS) in Normal Women and Women with High DS Concentrations^*

Brown University and Women and Infants Hospital Providence, Rhode Island 02905
University Hospital Clinical Laboratories and University of Wisconsin Madison Wisconsin
Departments of Obstetrics and Gynecology and Medicine, University of Massachusetts Medical School Worcester, Massachusetts 01605

Address all correspondence and requests for reprints to: Ray V. Haning, Jr., M.D. Department of Obstetrics and Gynecology, Women and Infants Hospital, 101 Dudley Street, Providence, Rhode Island 02905.

In order to determine the contribution of serum dehydroepiandrosterone sulfate (DS) to estrone (E₁) production in normal women and the effect of chronic elevation of the serum DS concentration on DS metabolism, four normal women and four women with high endogenous serum DS were infused with [³H]DS and [¹⁴C]E₁ or [¹⁴C]testosterone for 6 h. Blood samples were analyzed for radioactivity as DS, dehydroepiandrosterone (D), androstenedione, testosterone, and dihydrotestosterone. Urine was collected for analysis of creatinine, 17- ketosteroids (17–KS), and radioactivity as estrone (E₁). The serum DS of 12.4 ± 1.44 µmol/L (mean ± SE) in the group with high DS was higher than that of 3.96 ± 1.0 /nmol/L (1.46 ± 0.37 Mg/mL) in the normals (P < 0.005). Those with high DS also had increased 17-KS (13.2 ± 2.0 vs. 5.68 ± 0.68 mg/day, P < 0.025) and a higher blood production rate of DS () (126 ± 21 (n = 3) vs. 54.3 ± 13.8 mmol/day, P < 0.05) but a lower MCRDS (10.94 ± 0.61 (n = 3) vs. 13.8 ± 0.27 L/day, P < 0.01) than that in normals. In the four normal women the fraction of infused DS converted to estrone was 0.00078 ± 0.00018, the amount of E₁ produced from serum DS was 41.3 ± 15 nmol/day, the basal plasma E₁ was 102 ± 18 pmol/L, the MCREl was 1340 ± 181 L/day, the value for blood production of E₁ was 129 ± 12 nmol/day, and the portion of E₁ derived from DS was 30.4 ± 9.4%. Correlation analysis of the data from these eight subjects showed that 17-KS, , and the serum DS were all correlated with body surface area, body weight, and ponderal index and that 17-KS excretion, , and serum DS were all correlated with one another. The most important predictors of 17-KS excretion were serum DS (P < 0.001) and the ponderal index (P < 0.05).

^* This work was supported in part by NIH Grants R01-HD-21280 and 5-M01-RR-02038.

Received March 15, 1991.

This article has been cited by other articles:

				P. A. Komesaroff Unravelling the Enigma of Dehydroepiandrosterone: Moving Forward Step by Step Endocrinology, March 1, 2008; 149(3): 886 - 888. [Full Text] [PDF]

				L. Wang, Y.-D. Wang, W.-J. Wang, Y. Zhu, and D.-J. Li Dehydroepiandrosterone improves murine osteoblast growth and bone tissue morphometry via mitogen-activated protein kinase signaling pathway independent of either androgen receptor or estrogen receptor J. Mol. Endocrinol., April 1, 2007; 38(4): 467 - 479. [Abstract] [Full Text] [PDF]

				M. R. I. Williams, T. Dawood, S. Ling, A. Dai, R. Lew, K. Myles, J. W. Funder, K. Sudhir, and P. A. Komesaroff Dehydroepiandrosterone Increases Endothelial Cell Proliferation in Vitro and Improves Endothelial Function in Vivo by Mechanisms Independent of Androgen and Estrogen Receptors J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4708 - 4715. [Abstract] [Full Text] [PDF]

				M. R. I. Williams, S. Ling, T. Dawood, K. Hashimura, A. Dai, H. Li, J.-P. Liu, J. W. Funder, K. Sudhir, and P. A. Komesaroff Dehydroepiandrosterone Inhibits Human Vascular Smooth Muscle Cell Proliferation Independent of ARs and ERs J. Clin. Endocrinol. Metab., January 1, 2002; 87(1): 176 - 181. [Abstract] [Full Text] [PDF]

				S. Legrain, C. Massien, N. Lahlou, M. Roger, B. Debuire, B. Diquet, G. Chatellier, M. Azizi, V. Faucounau, H. Porchet, et al. Dehydroepiandrosterone Replacement Administration: Pharmacokinetic and Pharmacodynamic Studies in Healthy Elderly Subjects J. Clin. Endocrinol. Metab., September 1, 2000; 85(9): 3208 - 3217. [Abstract] [Full Text]

				W. Arlt, H.-G. Justl, F. Callies, M. Reincke, D. Hübler, M. Oettel, M. Ernst, H. M. Schulte, and B. Allolio Oral Dehydroepiandrosterone for Adrenal Androgen Replacement: Pharmacokinetics and Peripheral Conversion to Androgens and Estrogens in Young Healthy Females after Dexamethasone Suppression J. Clin. Endocrinol. Metab., June 1, 1998; 83(6): 1928 - 1934. [Abstract] [Full Text]