Low-grade metabolic acidosis may be the cause of sodium chloride-induced exaggerated bone resorption
Low-grade metabolic acidosis may be the cause of sodium chloride-induced exaggerated bone resorption
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DOI：
10.1359/jbmr.071118
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发表时间：
2008-04-01
影响因子：
6.2
通讯作者：
Heer, Martina
中科院分区：
文献类型：
--
作者：
Frings-Meuthen, Petra;Baecker, Natalie;Heer, Martina
健康男性受试者中NaCl摄入量的逐步增加导致轻度代谢性酸中毒。通过分析骨吸收标志物，我们研究了饮食中增加氯化钠（NaCl）对骨代谢和酸碱平衡的影响。材料和方法：受试者是9名健康男性（平均年龄，25.7 ± 3.1岁;平均体重[BW]，71.5 ± 4.0 kg）。在第一阶段（6天），受试者每天接受0.7 mEq NaCl/kg BW（阶段1），在第二阶段（6天）每天接受2.8 mEq NaCl/kg BW（阶段2），在第三阶段（10天）每天接受7.7 mEq NaCl/kg BW（阶段3），在第四阶段（6天）每天接受0.7 mEq NaCl/kg BW（阶段4）。随着NaCl摄入量的增加，24小时尿钙和钠排泄量显著增加（两者p < 0.001）。骨吸收标记物G和I型胶原N端肽（CTX，NTX）的尿排泄从2期增加到3期（CTX，p = 0.013; NTX，p < 0.001），从3期减少到4期（CTX，p < 0.001; NTX，p = 0.002）。骨形成标志物的N-末端前肽的I型前胶原，骨特异性碱性磷酸酶，骨钙素保持不变，从低到高氯化钠摄入量。第1阶段和第3阶段之间的血液pH值水平降低（p = 0.04）。血碳酸氢盐（HCO 3-）和碱过剩（BE）从第1阶段到第3阶段（两者均为p < 0.001）和从第2阶段到第3阶段（HCO 3-，p = 0.003; BE，p = 0.015）降低。几乎所有的骨吸收指标和酸碱变量在第4阶段都达到了基线水平。结论：我们得出结论，低度代谢性酸中毒可能是NaCl诱导的过度骨吸收的原因。
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 G 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.