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The Journal of Clinical Endocrinology & Metabolism Vol. 95, No. 10 4743-4747
Copyright © 2010 by The Endocrine Society
Testosterone Suppresses Hepcidin in Men: A Potential Mechanism for Testosterone-Induced Erythrocytosis
Eric Bachman, Rui Feng1, Thomas Travison1, Michelle Li, Gordana Olbina, Vaughn Ostland, Jagadish Ulloor, Anqi Zhang, Shehzad Basaria, Tomas Ganz, Mark Westerman and Shalender Bhasin
Department of Medicine (E.C., T.T., S.Ba., S.Bh., M.L., J.U., A.Z.), Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston, Massachusetts 02118; Department of Biostatistics and Epidemiology (R.F.), University of Pennsylvania, Philadelphia, Pennsylvania 19104; Medicine and Pathology (T.G.), CHS 37-055, Department of Medicine, David Geffen School of Medicine, Los Angeles, California 90095-1690; and Intrinsic LifeSciences LLC (M.W., G.O., V.O.), La Jolla, California 92037
Address all correspondence and requests for reprints to: Eric Bachman, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, 670 Albany Street, Boston, Massachusetts 02118. E-mail: [email protected].
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.
Copyright © 2010 by The Endocrine Society
Testosterone Suppresses Hepcidin in Men: A Potential Mechanism for Testosterone-Induced Erythrocytosis
Eric Bachman, Rui Feng1, Thomas Travison1, Michelle Li, Gordana Olbina, Vaughn Ostland, Jagadish Ulloor, Anqi Zhang, Shehzad Basaria, Tomas Ganz, Mark Westerman and Shalender Bhasin
Department of Medicine (E.C., T.T., S.Ba., S.Bh., M.L., J.U., A.Z.), Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston, Massachusetts 02118; Department of Biostatistics and Epidemiology (R.F.), University of Pennsylvania, Philadelphia, Pennsylvania 19104; Medicine and Pathology (T.G.), CHS 37-055, Department of Medicine, David Geffen School of Medicine, Los Angeles, California 90095-1690; and Intrinsic LifeSciences LLC (M.W., G.O., V.O.), La Jolla, California 92037
Address all correspondence and requests for reprints to: Eric Bachman, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, 670 Albany Street, Boston, Massachusetts 02118. E-mail: [email protected].
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.
