Parts of the results were previously presented at Experimental Biology 2005, San Diego, CA, USA, April 2–6, 2005.
Version of Record online: 3 DEC 2007
Copyright © 2008 ASBMR
Journal of Bone and Mineral Research
Volume 23, Issue 4, pages 517–524, April 2008
How to Cite
Frings-Meuthen, P., Baecker, N. and Heer, M. (2008), Low-Grade Metabolic Acidosis May Be the Cause of Sodium Chloride–Induced Exaggerated Bone Resorption. J Bone Miner Res, 23: 517–524. doi: 10.1359/jbmr.071118
The authors state that they have no conflicts of interest.
- Issue online: 4 DEC 2009
- Version of Record online: 3 DEC 2007
- Manuscript Accepted: 26 NOV 2007
- Manuscript Revised: 30 OCT 2007
- Manuscript Received: 14 MAY 2007
- metabolic ward;
- sodium chloride;
- acid-base balance
Stepwise increase in NaCl intake in healthy male test subjects led to a low-grade metabolic acidosis. This was most likely the cause for increased bone resorption during high sodium chloride intake, as determined by analyzing bone resorption markers.
Introduction: We examined the effect of increased dietary sodium chloride (NaCl) on bone metabolism and acid-base balance.
Materials and Methods: Subjects were nine healthy men (mean age, 25.7 ± 3.1 yr; mean body weight [BW], 71.5 ± 4.0 kg). During the first period (6 days), subjects received 0.7 mEq NaCl/kg BW per day (phase 1), during the second period (6 days) 2.8 mEq NaCl/kg BW per day (phase 2), during the third period (10 days) 7.7 mEq NaCl/kg BW per day (phase 3), and during the fourth period (6 days) 0.7 mEq NaCl/kg BW per day (phase 4).
Results: Twenty-four-hour urinary excretion of calcium and sodium rose significantly with increasing NaCl intake (p < 0.001 for both). Urinary excretion of bone resorption markers C- and N-terminal telopeptide of type I collagen (CTX, NTX) increased from phase 2 to phase 3 (CTX, p = 0.013; NTX, p < 0.001) and decreased from phase 3 to phase 4 (CTX, p < 0.001; NTX, p = 0.002). Bone formation markers N-terminal propeptide of type I procollagen, bone-specific alkaline phosphatase, and osteocalcin remained unchanged from low to high NaCl intake. Blood pH levels decreased (p = 0.04) between phases 1 and 3. Blood bicarbonate (HCO3−) and base excess (BE) decreased from phases 1 to 3 (p < 0.001 for both) and from phases 2–3 (HCO3−, p = 0.003; BE, p = 0.015). Nearly all bone resorption markers and acid-base variables reached their baseline levels in phase 4.
Conclusions: We conclude that low-grade metabolic acidosis may be the cause of NaCl-induced exaggerated bone resorption.