title: The effect of gonadotropin withdrawal and stimulation with human chorionic gonadotropin on intratesticular androstenedione and DHEA in normal men.
abstract: BACKGROUND
  Concentrations of intratesticular (IT) testosterone (T) are known to be 100-200 times those of serum T; however, the IT concentrations of T's precursors, their testicular to serum gradients, gonadotropin dependence, and response to stimulation with human chorionic gonadotropin (hCG) have not been studied in detail. We hypothesized that serum and IT androstenedione (ADD) and IT dehydroepiandrosterone (DHEA) would be significantly suppressed by the administration of a GnRH antagonist and increased when stimulated by hCG, without a similar suppression of serum DHEA.
  
  
  METHODS
  We suppressed gonadotropins in 23 normal men with the GnRH antagonist acyline and randomly assigned them to one of four doses of hCG, 0, 15, 60, or 125 IU sc every other day for 10 d. Blood and IT fluid for the measurement of serum and IT hormones were obtained at baseline and after 10 d of treatment.
  
  
  RESULTS
  Baseline IT ADD [median (25th, 75th percentile)] was 629 (308, 860) nmol/liter, and IT DHEA was 564 (411, 879) nmol/liter, which were 175 and 27 times higher than their respective serum concentrations. IT ADD and IT DHEA were suppressed by 98 and 82%, respectively, by acyline and significantly increased with hCG administration. Likewise, serum ADD was suppressed by 50%, but serum DHEA was unchanged.
  
  
  CONCLUSIONS
  ADD and DHEA are highly concentrated within the human testes compared with serum. Serum and IT ADD and IT DHEA are markedly suppressed with GnRH administration and stimulated by hCG, but serum DHEA is not, suggesting that most circulating DHEA is not of testicular origin.
authors.affiliation: Departments of Internal Medicine, University of Washington, Seattle, Washington 91895, USA. mylang@u.washington.edu
authors.forename: M Y
authors.initials: MY
authors.lastname: Roth
authors.forename: S T
authors.initials: ST
authors.lastname: Page
authors.forename: K
authors.initials: K
authors.lastname: Lin
authors.forename: B D
authors.initials: BD
authors.lastname: Anawalt
authors.forename: A M
authors.initials: AM
authors.lastname: Matsumoto
authors.forename: B
authors.initials: B
authors.lastname: Marck
authors.forename: W J
authors.initials: WJ
authors.lastname: Bremner
authors.forename: J K
authors.initials: JK
authors.lastname: Amory
mesh_terms: D000293:Adolescent; D000328:Adult; D000735:Androstenedione / Q000032:analysis / Q000378:metabolism*; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D003687:Dehydroepiandrosterone / Q000032:analysis / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006062:Gonadotropins / Q000494:pharmacology*; D006727:Hormone Antagonists / Q000494:pharmacology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009842:Oligopeptides / Q000494:pharmacology; D013268:Stimulation, Chemical; D013737:Testis / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism; D013739:Testosterone / Q000032:analysis / Q000378:metabolism; D028761:Withholding Treatment; D055815:Young Adult
chemical_list: D006063:Chorionic Gonadotropin; D006062:Gonadotropins; D006727:Hormone Antagonists; D009842:Oligopeptides; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; C109238:acyline