Cited by 247Iron Metabolism and DisordersHormonal and reproductive studiesErythropoietin and Anemia Treatment

Testosterone Suppresses Hepcidin in Men: A Potential Mechanism for Testosterone-Induced Erythrocytosis

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Bachman, Eric, Feng, Rui, Travison, Thomas, Li, Michelle, Olbina, Gordana, Ostland, Vaughn, Ulloor, Jagadish, Zhang, Anqi +4 more·2010·The Journal of Clinical Endocrinology & Metabolism

Abstract

CONTEXT: 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. PARTICIPANTS: 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. CONCLUSION: 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.

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Crossref · 10.1210/jc.2010-0864

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Authors
Bachman, E., Feng, R., Travison, T., Li, M., Olbina, G., Ostland, V., Ulloor, J., Zhang, A., Basaria, S., Ganz, T., Westerman, M., & Bhasin, S.
Affiliations
  • Boston University (US)
  • University of Pennsylvania (US)
  • Intrinsic LifeSciences (United States) (US)
  • University of California, Los Angeles (US)
Corresponding author
Bachman, Eric
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
2010-10
Volume
95
Issue
10
Pages
4743-4747
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
OpenAlex
W2150542348
Cited by
247
References
19
Citations by year
2026: 18 · 2025: 14 · 2024: 9 · 2023: 16 · 2022: 16 · 2021: 11 · 2020: 23 · 2019: 15 · 2018: 13 · 2017: 18 · 2016: 12 · 2015: 20 · 2014: 15 · 2013: 20 · 2012: 16
FWCI
9.41
Type
journal article
Language
en
Open access
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • School of Medicine, Boston University
  • Evans Medical Foundation
  • National Institutes of Health (5p30ag031679-15)
  • National Institute on Aging (U01AG014369, U01 AG14369, P30-AG031679)
Topics
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
  • Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
Keywords
testosterone, hepcidin, testosterone enanthate, hematocrit, hemoglobin, iron regulation, GnRH agonist suppression, dose-response relationship, age differences, men
MeSH terms
Adult, Aged, Aging, Dose-Response Relationship, Drug, Double-Blind Method, Drug Administration Schedule, Humans, Injections, Male, Middle Aged, Polycythemia, Testosterone, Down-Regulation, Leuprolide, Antimicrobial Cationic Peptides, Young Adult, Hepcidins

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