title: Testosterone suppresses hepcidin in men: a potential mechanism for testosterone-induced erythrocytosis.
abstract: BACKGROUND
  The mechanisms by which testosterone increases hemoglobin and hematocrit are unknown.
  
  
  OBJECTIVE
  The aim was to test the hypothesis that testosterone-induced increase in hematocrit is associated with suppression of the iron regulatory peptide hepcidin.
  
  
  METHODS
  Healthy younger men (ages 19-35 yr; n = 53) and older men (ages 59-75 yr; n = 56) were studied.
  
  
  METHODS
  Weekly doses of testosterone enanthate (25, 50, 125, 300, and 600 mg) were administered over 20 wk, whereas endogenous testosterone was suppressed by monthly GnRH agonist administration. Blood and serum parameters from each individual were measured at wk 0, 1, 2, 4, 8, and 20. Longitudinal analyses were performed to examine the relationship between hepcidin, hemoglobin, hematocrit, and testosterone while controlling for potential confounders.
  
  
  RESULTS
  High levels of testosterone markedly suppressed serum hepcidin within 1 wk. Hepcidin suppression in response to testosterone administration was dose-dependent in older men and more pronounced than in young men, and this corresponded to a greater rise in hemoglobin in older men. Serum hepcidin levels at 4 and 8 wk were predictive of change in hematocrit from baseline to peak levels.
  
  
  CONCLUSIONS
  Testosterone administration is associated with suppression of serum hepcidin. Greater increases in hematocrit in older men during testosterone therapy are related to greater suppression of hepcidin.
authors.affiliation: Department of Medicine, Boston University School of Medicine, 670 Albany Street, Boston, Massachusetts 02118, USA. eric.bachman@bmc.org
authors.forename: Eric
authors.initials: E
authors.lastname: Bachman
authors.forename: Rui
authors.initials: R
authors.lastname: Feng
authors.forename: Thomas
authors.initials: T
authors.lastname: Travison
authors.forename: Michelle
authors.initials: M
authors.lastname: Li
authors.forename: Gordana
authors.initials: G
authors.lastname: Olbina
authors.forename: Vaughn
authors.initials: V
authors.lastname: Ostland
authors.forename: Jagadish
authors.initials: J
authors.lastname: Ulloor
authors.forename: Anqi
authors.initials: A
authors.lastname: Zhang
authors.forename: Shehzad
authors.initials: S
authors.lastname: Basaria
authors.forename: Tomas
authors.initials: T
authors.lastname: Ganz
authors.forename: Mark
authors.initials: M
authors.lastname: Westerman
authors.forename: Shalender
authors.initials: S
authors.lastname: Bhasin
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000097:blood / Q000502:physiology; D023181:Antimicrobial Cationic Peptides / Q000097:blood* / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D015536:Down-Regulation / Q000187:drug effects; D004334:Drug Administration Schedule; D064451:Hepcidins; D006801:Humans; D007267:Injections; D016729:Leuprolide / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D011086:Polycythemia / Q000139:chemically induced*; D013739:Testosterone / Q000008:administration & dosage / Q000494:pharmacology*; D055815:Young Adult
chemical_list: D023181:Antimicrobial Cationic Peptides; C578702:HAMP protein, human; D064451:Hepcidins; D013739:Testosterone; D016729:Leuprolide