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，人体的主要钙储备，进入尿液。在英年华 男性和女性，这种盐诱导的骨骼钙丢失会导致 甲状旁腺和维生素D活性的稳态调节 增加肠道对膳食钙的吸收。这种内分泌学- 老年受试者的胃肠道反应似乎受损。在……里面 因此，绝经后妇女长期摄入过量的钠 氯化物可能导致持续的未补偿的尿钙损失 和异常高的骨吸收率，并导致 骨质疏松的发病机制。盐引起的尿钙丢失和 补充剂可防止骨吸收率的增加 日粮中含有碳酸氢钾，一种可吸收的碱盐 强效的抗钙尿特性。我们将在绝经后确定 女性盐源性高钙尿症是否真的与 使用高度特异的现代生化技术，提高骨骼的转换率 骨吸收和骨形成的标志物；骨的变化 研究对象之间的更替是通过变化或缺乏变化来预测的， 在副激素-维生素D轴上；以及慢性补充剂是否 日粮中添加碳酸氢钾可预防盐中毒 高钙尿症和骨转换增加。在这个随机的，双重的- 双盲、安慰剂对照研究，绝经后妇女(n=50)将 首先适应低盐饮食(70-90meq/天)三周，然后 随机分为两个治疗组(每组25人)：(A) 高盐饮食(210-230meq/天)加安慰剂，或(B)高盐饮食 (210-230meq/d)，添加碳酸氢钾(90 mmol/d)，用于 四周。在每个研究周期后，尿钙、环磷酸腺苷、 骨吸收标记物(脱氧吡啶，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 从而将决定绝经后妇女的食盐是否作为一种 高钙尿剂，刺激骨吸收，到什么程度 这种影响可以通过内分泌稳态机制来缓解，并且 饮食中是否长期补充碳酸氢钾 将防止盐诱导的高钙尿和增加的骨吸收。

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.