发表机构
Polytechnic University of Puerto Rico; Universidad Nacional Politécnica Antonio José de Sucre (UNEXPO)（波多黎各理工大学; 安东尼奥·何塞·德·苏克雷国立理工学院）
机构由 AI 辅助整理，请以论文原文为准。AI 中文总结
该研究提出一种整合骨密度、维生素D和PTH反应的临床-代谢模型及四步决策算法，以精准评估个体钙需求，预防继发性甲旁亢并避免过度补充。
AI 中文摘要
钙稳态由包含甲状旁腺激素（PTH）、骨化三醇和降钙素的内分泌网络维持，该网络以牺牲骨骼储备为代价来保护血清钙。因此，血清钙是营养性钙状态不可靠的指标，经验性补充仍然常见。本叙述性综述提出了一种估计个体钙需求的临床-代谢方法，该方法整合了骨矿物质密度（BMD）、维生素D状态和代偿性PTH反应。我们做出三项贡献。首先，我们提出了一个S形磷酸盐-PTH模型，其中葡萄糖依赖性增益项（$\Delta k_{\mathrm{gluc}}$）捕捉与血糖异常相关的甲状旁腺敏感性增高，并用健康成年人、女性和糖性骨质疏松症患者的模拟值进行了说明。其次，我们将该模型转化为一个四步决策算法，将摄入缺口定义为肠道吸收、肾脏排泄和骨转换的净平衡。第三，我们纳入骨细胞-成骨细胞生物能量轴（硬骨素/Wnt信号、GLUT1介导的葡萄糖摄取、有氧糖酵解和骨钙素-胰岛素串扰）来解释当细胞能量供应或胰岛素敏感性受损时钙补充可能无效的原因。该框架旨在预防继发性甲状旁腺功能亢进、避免过度补充并保持骨骼完整性。模型值为模拟值，需要前瞻性临床验证。
英文摘要
Calcium homeostasis is maintained by an endocrine network comprising parathyroid hormone (PTH), calcitriol and calcitonin, which defends serum calcium at the expense of skeletal reserves. Serum calcium is therefore an unreliable indicator of nutritional calcium status, and empirical supplementation remains common. This narrative review proposes a clinical--metabolic approach to estimating individual calcium requirements that integrates bone mineral density (BMD), vitamin D status and the compensatory PTH response. We make three contributions. First, we present a sigmoidal phosphate--PTH model in which a glucose-dependent gain term ($Δk_{\mathrm{gluc}}$) captures the heightened parathyroid sensitivity associated with dysglycaemia, and we illustrate it with simulated values for healthy adults, women and individuals with gluco-osteoporosis. Second, we translate the model into a four-step decision algorithm that frames the intake gap as a net balance of intestinal absorption, renal excretion and bone turnover. Third, we incorporate the osteocyte--osteoblast bioenergetic axis (sclerostin/Wnt signalling, GLUT1-mediated glucose uptake, aerobic glycolysis and osteocalcin--insulin crosstalk) to explain why calcium supplementation may be ineffective when cellular energy supply or insulin sensitivity is impaired. The framework aims to prevent secondary hyperparathyroidism, avoid over supplementation and preserve skeletal integrity. The model values are simulated and require prospective clinical validation.
Comments5 pages, 1 figure
