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Am J Physiol Endocrinol Metab. 2014 Sep 1;307(5):E456-61. doi: 10.1152/ajpendo.00184.2014. Epub 2014 Jul 29.

Testosterone alters iron metabolism and stimulates red blood cell production independently of dihydrotestosterone.

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Research Service, Departments of Applied Physiology and Kinesiology.
Research Service.
Geriatric Research, Education, and Clinical Center, and.
Department of Kinesiology, University of Rhode Island, Kingston, Rhode Island.
Research Pharmacy, Malcom Randall Veterans Affairs Medical Center, University of Florida, Gainesville, Florida;
Biostatistics, and.
Health Outcomes and Policy, University of Florida, Gainesville, Florida; and.
Geriatric Research, Education, and Clinical Center, and Departments of Applied Physiology and Kinesiology,


Testosterone (T) stimulates erythropoiesis and regulates iron homeostasis. However, it remains unknown whether the (type II) 5α-reduction of T to dihydrotestosterone (DHT) mediates these androgenic effects, as it does in some other tissues. Our purpose was to determine whether inhibition of type II 5α-reductase (via finasteride) alters red blood cell (RBC) production and serum markers of iron homeostasis subsequent to testosterone-enanthate (TE) administration in older hypogonadal men. Sixty men aged ≥60 yr with serum T <300 ng/dl or bioavailable T <70 ng/dl received treatment with TE (125 mg/wk) vs. vehicle paired with finasteride (5 mg/day) vs. placebo using a 2 × 2 factorial design. Over the course of 12 mo, TE increased RBC count 9%, hematocrit 4%, and hemoglobin 8% while suppressing serum hepcidin 57% (P < 0.001 for all measurements). Most of the aforementioned changes occurred in the first 3 mo of treatment, and finasteride coadministration did not significantly alter any of these effects. TE also reduced serum ferritin 32% (P = 0.002) within 3 mo of treatment initiation without altering iron, transferrin, or transferrin saturation. We conclude that TE stimulates erythropoiesis and alters iron homeostasis independently of the type II 5α-reductase enzyme. These results demonstrate that elevated DHT is not required for androgen-mediated erythropoiesis or for alterations in iron homeostasis that would appear to support iron incorporation into RBCs.


androgen; finasteride; hematocrit; hepcidin; hypogonadal; testosterone

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