In:
American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 306, No. 4 ( 2014-02-15), p. E433-E442
Abstract:
Testosterone acts directly at androgen receptors and also exerts potent actions following 5α-reduction to dihydrotestosterone (DHT). Finasteride (type II 5α-reductase inhibitor) lowers DHT and is used to treat benign prostatic hyperplasia. However, it is unknown whether elevated DHT mediates either beneficial musculoskeletal effects or prostate enlargement resulting from higher-than-replacement doses of testosterone. Our purpose was to determine whether administration of testosterone plus finasteride to older hypogonadal men could produce musculoskeletal benefits without prostate enlargement. Sixty men aged ≥60 yr with a serum testosterone concentration of ≤300 ng/dl or bioavailable testosterone ≤70 ng/dl received 52 wk of treatment with testosterone enanthate (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 upper and lower body muscle strength by 8–14% ( P = 0.015 to 〈 0.001), fat-free mass 4.04 kg ( P = 0.032), lumbar spine bone mineral density (BMD) 4.19% ( P 〈 0.001), and total hip BMD 1.96% ( P = 0.024) while reducing total body fat −3.87 kg ( P 〈 0.001) and trunk fat −1.88 kg ( P = 0.0051). In the first 3 mo, testosterone increased hematocrit 4.13% ( P 〈 0.001). Coadministration of finasteride did not alter any of these effects. Over 12 mo, testosterone also increased prostate volume 11.4 cm 3 ( P = 0.0051), an effect that was completely prevented by finasteride ( P = 0.0027). We conclude that a higher-than-replacement TE combined with finasteride significantly increases muscle strength and BMD and reduces body fat without causing prostate enlargement. These results demonstrate that elevated DHT mediates testosterone-induced prostate enlargement but is not required for benefits in musculoskeletal or adipose tissue.
Type of Medium:
Online Resource
ISSN:
0193-1849
,
1522-1555
DOI:
10.1152/ajpendo.00592.2013
Language:
English
Publisher:
American Physiological Society
Publication Date:
2014
detail.hit.zdb_id:
1477331-4
SSG:
12
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