内分泌学
低磷血症
高磷血症
内科学
甲状旁腺激素
骨化三醇
钙
维生素D与神经学
化学
骨软化症
佝偻病
磷酸盐
成纤维细胞生长因子23
维生素D缺乏
维生素
钙代谢
医学
生物化学
作者
Nuraly S. Akimbekov,Ilya Digel,Dinara K. Sherelkhan,Mohammed S. Razzaque
标识
DOI:10.1007/978-3-030-91623-7_5
摘要
Vitamin D plays an essential role in calcium and inorganic phosphate (Pi) homeostasis, maintaining their optimal levels to assure adequate bone mineralization. Vitamin D, as calcitriol (1,25(OH)2D), not only increases intestinal calcium and phosphate absorption but also facilitates their renal reabsorption, leading to elevated serum calcium and phosphate levels. The interaction of 1,25(OH)2D with its receptor (VDR) increases the efficiency of intestinal absorption of calcium to 30-40% and phosphate to nearly 80%. Serum phosphate levels can also influence 1,25(OH)2D and fibroblast growth factor 23 (FGF23) levels, i.e., higher phosphate concentrations suppress vitamin D activation and stimulate parathyroid hormone (PTH) release, while a high FGF23 serum level leads to reduced vitamin D synthesis. In the vitamin D-deficient state, the intestinal calcium absorption decreases and the secretion of PTH increases, which in turn causes the stimulation of 1,25(OH)2D production, resulting in excessive urinary phosphate loss. Maintenance of phosphate homeostasis is essential as hyperphosphatemia is a risk factor of cardiovascular calcification, chronic kidney diseases (CKD), and premature aging, while hypophosphatemia is usually associated with rickets and osteomalacia. This chapter elaborates on the possible interactions between vitamin D and phosphate in health and disease.
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