Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice
Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice
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DOI：
10.1210/en.139.10.4391
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发表时间：
1998-10-01
期刊：
影响因子：
4.8
通讯作者：
Demay, MB
中科院分区：
文献类型：
--
作者：
Li, YC;Amling, M;Demay, MB
1,25-二羟基维生素D-3在肠道钙转运中起重要作用。为了确定在维生素D受体（VDR）消融小鼠中观察到的表型异常是继发于肠道钙吸收受损而不是受体缺乏，通过饮食手段使矿物质离子水平正常化。vdr切除的小鼠和对照组的同伴被喂食一种饮食，这种饮食已被证明可以预防维生素d缺乏大鼠的继发性甲状旁腺功能亢进。这种饮食使vdr消融小鼠的生长和随机血清电离钙水平正常化。离子钙水平的校正阻止甲状旁腺增生的发展和PTH信使RNA合成和血清PTH水平的增加。vdr消融动物喂食这种饮食没有发展佝偻病或骨软化。然而，在矿物质离子正常的VDR消融小鼠中仍然观察到脱发，这表明VDR是正常头发生长所必需的。该研究表明，在缺乏1,25-二羟基维生素D-3的基因组作用的情况下，矿物质离子稳态的正常化可以预防甲状旁腺功能亢进、骨软化和佝偻病的发展。
1,25-Dihydroxyvitamin D-3 plays a major role in intestinal calcium transport. To determine what phenotypic abnormalities observed in vitamin D receptor (VDR)-ablated mice are secondary to impaired intestinal calcium absorption rather than receptor deficiency, mineral ion levels were normalized by dietary means. VDR-ablated mice and control littermates were fed a diet that has been shown to prevent secondary hyperparathyroidism in vitamin D-deficient rats. This diet normalized growth and random serum ionized calcium levels in the VDR-ablated mice. The correction of ionized calcium levels prevented the development of parathyroid hyperplasia and the increases in PTH messenger RNA synthesis and in serum PTH levels. VDR-ablated animals fed this diet did not develop rickets or osteomalacia. However, alopecia was still observed in the VDR-ablated mice with normal mineral ions, suggesting that the VDR is required for normal hair growth. This study demonstrates that normalization of mineral ion homeostasis can prevent the development of hyperparathyroidism, osteomalacia, and rickets in the absence of the genomic actions of 1,25-dihydroxyvitamin D-3.