Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI109536

Concentration of Dihydrotestosterone and 3α-Androstanediol in Naturally Occurring and Androgen- Induced Prostatic Hyperplasia in the Dog

Ronald J. Moore, John M. Gazak, James F. Quebbeman, and Jean D. Wilson

Department of Internal Medicine and The Eugene McDermott Center for Growth and Development, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Find articles by Moore, R. in: JCI | PubMed | Google Scholar

Department of Internal Medicine and The Eugene McDermott Center for Growth and Development, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Find articles by Gazak, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine and The Eugene McDermott Center for Growth and Development, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Find articles by Quebbeman, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine and The Eugene McDermott Center for Growth and Development, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Find articles by Wilson, J. in: JCI | PubMed | Google Scholar

Published October 1, 1979 - More info

Published in Volume 64, Issue 4 on October 1, 1979
J Clin Invest. 1979;64(4):1003–1010. https://doi.org/10.1172/JCI109536.
© 1979 The American Society for Clinical Investigation
Published October 1, 1979 - Version history
View PDF
Abstract

Previous studies have suggested that dihydrotestosterone accumulation in the prostate may be involved in the pathogenesis of prostatic hyperplasia in man and dog. However, the fact that the administration of 10 mg dihydrotestosterone/d to castrated, mongrel dogs (0.5 mg/kg body wt) causes little growth in the prostate, whereas identical doses of 3α- androstanediol regularly induce prostatic hyperplasia (> 14 g weight) has raised the possibility that the dihydrotestosterone accumulation may be the result rather than the cause of the pathology. To investigate the mechanism of this phenomenon, we measured the levels of dihydrotestosterone and 3α-androstanediol in prostates from 75 dogs. In both naturally occurring and 3α-androstanediol-induced prostatic hyperplasia, the levels of dihydrotestosterone were high (>5 ng/g), whereas in immature glands and glands from dihydrotestosterone-treated animals, levels were similar (2.1 and 2.6 ng/g, respectively). 3α-Androstanediol levels were no different in animals treated with dihydrotestosterone or 3α-androstanediol.

Therefore, because exogenous 3α-androstanediol is a better precursor of prostatic dihydrotestosterone than exogenous dihydrotestosterone itself, the effects of treatment with larger doses (2.5 mg/kg per d) of dihydrotestosterone and 3α-androstanediol for 12 wk were examined. In these amounts, dihydrotestosterone was as effective as 3α-androstanediol in inducing the development of prostatic hyperplasia and in elevating prostatic dihydrotestosterone concentration.

Because dihydrotestosterone accumulates in spontaneous prostatic hyperplasia, because the administration of sufficient amounts of dihydrotestosterone to the castrated dog can induce the development of prostatic hyperplasia, and because 3α-androstanediol induces the development of hyperplasia via conversion to dihydrotestosterone, we conclude that accumulation of dihydrotestosterone is the cause of canine prostatic hyperplasia.

Images.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 1003
page 1003
icon of scanned page 1004
page 1004
icon of scanned page 1005
page 1005
icon of scanned page 1006
page 1006
icon of scanned page 1007
page 1007
icon of scanned page 1008
page 1008
icon of scanned page 1009
page 1009
icon of scanned page 1010
page 1010
Version history
  • Version 1 (October 1, 1979): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts