KHCO3 PREVENTS NACL INDUCED BONE RESORPTION IN HUMANS?

含有大量氯化钠的饮食会导致钙的流失 从骨骼，人体主要的钙储备，进入尿液。 年轻 无论男女，这种盐引起的骨骼钙流失导致 甲状旁腺和维生素D活性的稳态调节， 增加肠道对膳食钙吸收。 内分泌- 胃肠道反应似乎在老年受试者中受损。 在 因此，绝经后妇女长期摄入大量的钠 氯化物可能导致持续的非代偿性尿钙丢失 和异常高的骨吸收率，并有助于 骨质疏松症的发病机制。 盐引起的尿钙丢失和 骨吸收率的增加可以通过补充 碳酸氢钾是一种可吸收的碱性盐， 有效的抗钙尿特性。 我们将确定绝经后 女性盐诱导的高钙尿症是否与 增加骨转换，使用高度特异性的现代生化 骨吸收和骨形成的标志物;骨吸收和骨形成的变化是否 受试者之间的更替是通过变化来预测的，或者缺乏变化， 维生素D轴;以及是否长期补充 日粮中添加碳酸氢钾可预防盐诱导的 高钙尿症和骨转换增加。在这个随机的，双- 一项设盲、安慰剂对照研究，绝经后女性（n=50）将 首先适应低盐饮食（70-90 meq/天）三周，然后 随机分配至两个治疗组之一（每组n=25名受试者）：（a） 高盐饮食（210-230 meq/天）与安慰剂，或（B）高盐饮食 （210-230 meq/天），加入碳酸氢钾（90 mmol/天）， 四周。 在每个研究阶段后，尿钙，环磷酸腺苷， 骨吸收标志物（脱氧吡啶啉、N-端肽）和血清 甲状旁腺激素、骨化三醇和骨形成标志物 （骨钙素，I型胶原前肽）将被测量。 本研究 因此，将决定在绝经后妇女是否饮食盐，作为一个 高钙尿剂，刺激骨吸收，到什么程度， 影响可通过内分泌稳态机制减轻， 饮食中长期补充碳酸氢钾 将防止盐引起的高钙尿症和增加的骨吸收。

Diets containing abundant sodium chloride lead to a drain of calcium from bone, the body's major calcium reserve, into the urine. In young men and women, this salt-induced loss of skeletal calcium leads to homeostatic adjustments of parathyroid and vitamin D activity that increase intestinal absorption of dietary calcium. This endocrinologic- gastrointestinal response appears to be impaired in older subjects. In postmenopausal women, therefore, chronic ingestion of abundant sodium chloride might lead to sustained uncompensated urinary calcium losses and abnormally high rates of bone resorption, and contribute to the pathogenesis of osteoporosis. Salt-induced urinary calcium losses and increases in bone resorption rate might be prevented by supplementation of the diet with potassium bicarbonate, an absorbable alkali salt with potent anti-calciuric properties. We will determine in postmenopausal women whether salt-induced hypercalciuria is truly associated with increased bone turnover, using highly specific modern biochemical markers of bone resorption and formation; whether the changes in bone turnover among subjects are predicted by the changes, or lack thereof, in the parahormone-vitamin D axis; and whether chronic supplementation of the diet with potassium bicarbonate can prevent salt-induced hypercalciuria and increased bone turnover. In this randomized, double- blinded, placebo-controlled study, postmenopausal women (n=50) will be first adapted to a low salt diet (70-90 meq/day) for three weeks then randomized to one of two treatment groups (n=25 subjects each): (a) high-salt diet (210-230 meq/day) with placebo, or (b) high-salt diet (210-230 meq/day) with added potassium bicarbonate (90 mmol/day) for four weeks. After each study period, urinary calcium, cyclic AMP, markers of bone resorption (deoxypyridinoline, N-telopeptide); and serum parathyroid hormone, calcitriol, and markers of bone formation (osteocalcin, type I collagen propeptide) will be measured. This study thus will determine in postmenopausal women whether dietary salt, as a hypercalciuric agent, stimulates bone resorption, to what extent that effect may be mitigated by endocrinologic homeostatic mechanisms, and whether chronic supplementation of the diet with potassium bicarbonate will prevent salt-induced hypercalciuria and increased bone resorption.