{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T04:39:55Z","timestamp":1779165595892,"version":"3.51.4"},"reference-count":40,"publisher":"The Endocrine Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The prostate strongly expresses type 2 5\u03b1-reductase, which avidly converts on entry most testosterone (T) to 5\u03b1-dihydrotestosterone (DHT). However, the quantitative contribution of the prostate to blood DHT is uncertain. We evaluated prostatic contribution to blood DHT by comparing the blood DHT concentrations in androgen-deficient patients with or without a prostate while they were receiving standard dose of T replacement. Androgen-deficient males (ADM) and female to male (F2M) transsexuals were studied in 2 centers, with both groups receiving either testosterone ester injections (250 mg mixed T esters) every 1 wk (Amsterdam) or 800 mg subdermal T implantation (Sydney). Among 39 Dutch patients, F2M (n = 21) were younger and smaller in physique than ADM (n = 18). One week (\u00b11 d) after an injection, plasma DHT concentrations were 1.6 \u00b1 0.2 (F2M) vs. 1.4 \u00b1 0.2 (ADM) nmol\/liter (P = 0.47), but the postinjection time interval to blood sampling was shorter in F2M (5.9 \u00b1 0.4 vs. 7.2 \u00b1 0.3 d; P = 0.01). Covariance adjustment for time since last injection, age, and physique did not change the lack of significant difference in postinjection plasma DHT concentration. The rapid and wide excursions in plasma T concentrations after an im T ester injection make the timing of blood sampling critical. To remove confounding by this variable, the experiment was repeated at a second site in similar patients, but using a depot T that achieves steady-state delivery for prolonged periods. Among 29 Australian patients, before and 1 month after subdermal implantation of 800 mg T, plasma DHT concentrations were not significantly different between groups [F2M, 1.1 \u00b1 0.1 (n = 14); ADM, 1.3 \u00b1 0.1 (n = 15); P = 0.28]. Correction for covariates, including age, height, weight, body surface area, and body mass index, did not influence the lack of significant difference between treated groups. As both modes of T administration yielded similar plasma DHT concentrations regardless of the presence of a prostate, this study indicates that the normal human prostate is not a major contributor to circulating blood DHT concentrations.<\/jats:p>","DOI":"10.1210\/jc.2003-030521","type":"journal-article","created":{"date-parts":[[2003,11,6]],"date-time":"2003-11-06T13:11:05Z","timestamp":1068124265000},"page":"5207-5211","source":"Crossref","is-referenced-by-count":22,"title":["Estimating the Contribution of the Prostate to Blood Dihydrotestosterone"],"prefix":"10.1210","volume":"88","author":[{"given":"Arno W. F. T.","family":"Toorians","sequence":"first","affiliation":[{"name":"Department of Endocrinology\/Andrology, Vrije Universiteit University Medical Center (A.W.F.T.T., L.J.G.), 1007 MB Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sharyn","family":"Kelleher","sequence":"additional","affiliation":[{"name":"Department of Andrology, Concord Hospital and ANZAC Research Institute, University of Sydney (S.K., M.J., D.J.H.), Sydney, New South Wales 2139, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Louis J.","family":"Gooren","sequence":"additional","affiliation":[{"name":"Department of Endocrinology\/Andrology, Vrije Universiteit University Medical Center (A.W.F.T.T., L.J.G.), 1007 MB Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark","family":"Jimenez","sequence":"additional","affiliation":[{"name":"Department of Andrology, Concord Hospital and ANZAC Research Institute, University of Sydney (S.K., M.J., D.J.H.), Sydney, New South Wales 2139, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David J.","family":"Handelsman","sequence":"additional","affiliation":[{"name":"Department of Andrology, Concord Hospital and ANZAC Research Institute, University of Sydney (S.K., M.J., D.J.H.), Sydney, New South Wales 2139, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"80","reference":[{"key":"2020071613323321900_R1","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1146\/annurev.bi.63.070194.000325","article-title":"Steroid 5\u03b1-reductase: two genes\/two enzymes.","volume":"63","author":"Russell","year":"1994","journal-title":"Annu Rev Biochem"},{"key":"2020071613323321900_R2","doi-asserted-by":"crossref","first-page":"17","DOI":"10.1016\/S0090-4295(01)01299-7","article-title":"5\u03b1-Reductase activity in the prostate.","volume":"58","author":"Steers","year":"2001","journal-title":"Urology"},{"key":"2020071613323321900_R3","doi-asserted-by":"crossref","first-page":"75","DOI":"10.1016\/S0960-0760(00)00139-4","article-title":"Enzyme assay for 5\u03b1-reductase type 2 activity in the presence of 5\u03b1-reductase type 1 activity in rat testis.","volume":"75","author":"Pratis","year":"2000","journal-title":"J Steroid Biochem Mol Biol"},{"key":"2020071613323321900_R4","first-page":"33","article-title":"The androgen receptor: physiology and pathyphysiology","author":"Quigley","year":"1998","journal-title":"In: Nieschlag E, Behre HM, eds. 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