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

Author:

Beggs Luke A.12,Yarrow Joshua F.12,Conover Christine F.1,Meuleman John R.3,Beck Darren T.4,Morrow Matthew5,Zou Baiming6,Shuster Jonathan J.7,Borst Stephen E.32

Affiliation:

1. Research Service,

2. Departments of 4Applied Physiology and Kinesiology,

3. Geriatric Research, Education, and Clinical Center, and

4. Department of Kinesiology, University of Rhode Island, Kingston, Rhode Island

5. Research Pharmacy, Malcom Randall Veterans Affairs Medical Center, University of Florida, Gainesville, Florida;

6. Biostatistics, and

7. Health Outcomes and Policy, University of Florida, Gainesville, Florida; and

Abstract

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.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism

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