The authors have no conflict of interest.
L-Arginine, the Natural Precursor of NO, Is Not Effective for Preventing Bone Loss in Postmenopausal Women†
Article first published online: 29 NOV 2004
Copyright © 2005 ASBMR
Journal of Bone and Mineral Research
Volume 20, Issue 3, pages 471–479, March 2005
How to Cite
Baecker, N., Boese, A., Schoenau, E., Gerzer, R. and Heer, M. (2005), L-Arginine, the Natural Precursor of NO, Is Not Effective for Preventing Bone Loss in Postmenopausal Women. J Bone Miner Res, 20: 471–479. doi: 10.1359/JBMR.041121
- Issue published online: 4 DEC 2009
- Article first published online: 29 NOV 2004
- Manuscript Accepted: 19 OCT 2004
- Manuscript Revised: 6 SEP 2004
- Manuscript Received: 7 APR 2004
- bone QCT;
- bone turnover markers
NO is an important regulator of bone turnover. L-Arginine, the natural precursor of NO, can enhance NO production. However, no effect of L-arginine hydrochloride supplementation was found on bone metabolism or on BMD, bone mass, or bone structure of healthy postmenopausal women.
Introduction: Recent studies indicate that NO exerts an anabolic effect on bone cell activity. The NO level of the human body can be elevated by administering pharmacological NO donors. Animal studies and the first human trial showed that NO donor administration had a positive effect on bone formation and a negative effect on bone resorption. L-arginine, the natural precursor of NO, can enhance NO production. This study was conducted to examine the effect of an oral L-arginine supplement on bone metabolism of healthy postmenopausal women.
Materials and Methods: The participants in this study were 30 healthy, age-matched postmenopausal women, divided into two groups. For 6 months, one group (54.5 ± 4.1 years; 66.3 ± 10.5 kg) received a daily oral supplement with 18 g L-arginine hydrochloride (14.8 g free L-arginine). The other 15 volunteers (55.3 ± 4.4 years; 64.2 ± 9.1 kg) received 18 g dextrose as a placebo. To verify compliance, 24-h urinary excretion of nitrogen was analyzed for 2 consecutive days at baseline and after 2, 4, and 6 months. At baseline and after 2, 4, and 6 months of supplementation, blood was drawn for analysis of insulin-like growth factor-I (IGF-I) and biomarkers of bone metabolism. At baseline, after 6 months, and after 1 year, pQCT measurements were performed at trabecular and cortical sites of the radius and tibia. The two groups of subjects were compared by repeated measures ANOVA.
Results: As expected, in the group with L-arginine hydrochloride supplementation, nitrogen excretion rose, and in the placebo group, it remained constant. Only bone formation marker, procollagen type I propeptides (PICP), increased significantly (p < 0.05) after 6 months of L-arginine supplementation. The results from pQCT showed no significant changes at any site in either group. No significant change in IGF-I concentration, which might have been caused by the L-arginine hydrochloride supplementation, was evident.
Conclusions: We conclude from these results that supplementation with L-arginine hydrochloride is not effective for improving bone mass in humans.