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Testosterone prevents protein loss via the hepatic urea cycle in human


CONTEXT: The urea cycle is a rate-limiting step for amino acid nitrogen elimination. The rate of urea synthesis is a true indicator of whole-body protein catabolism. Testosterone reduces protein and nitrogen loss. The effect of testosterone on hepatic urea synthesis in humans has not been studied. OBJECTIVE: To determine whether testosterone reduces hepatic urea production. DESIGN: An open-label study. PATIENTS AND INTERVENTION: Eight hypogonadal men were studied at baseline, and after two weeks of transdermal testosterone replacement (Testogel, 100 mg/day). MAIN OUTCOMES MEASURES: The rate of hepatic urea synthesis was measured by the urea turnover technique using stable isotope methodology, with (15)N2-urea as tracer. Whole-body leucine turnover was measured, from which leucine rate of appearance (LRa), an index of protein breakdown and leucine oxidation (Lox), a measure of irreversible protein loss, were calculated. RESULTS: Testosterone administration significantly reduced the rate of hepatic urea production (from 544.4 +/- 71.8 to 431.7 +/- 68.3 micromol/min; P < 0.01), which was paralleled by a significant reduction in serum urea concentration. Testosterone treatment significantly reduced net protein loss, as measured by percent Lox/LRa, by 19.3 +/- 5.8% (P < 0.05). There was a positive association between Lox and hepatic urea production at baseline (r(2) = 0.60, P < 0.05) and after testosterone administration (r(2) = 0.59, P < 0.05). CONCLUSION: Testosterone replacement reduces protein loss and hepatic urea synthesis. We conclude that testosterone regulates whole-body protein metabolism by suppressing the urea cycle.

Type Journal
ISBN 1479-683X (Electronic) 0804-4643 (Linking)
Authors Lam, T.; Poljak, A.; McLean, M.; Bahl, N.; Ho, K. K.; Birzniece, V.
Responsible Garvan Author (missing name)
Published Date 2017-04-17
Published Volume 176
Published Issue 4
Published Pages 489-496
Status Published in-print
DOI 10.1530/EJE-16-0868
URL link to publisher's version
OpenAccess link to author's accepted manuscript version