O'Doherty P J, DeLuca H F, Eicher E M
Endocrinology. 1977 Oct;101(4):1325-30. doi: 10.1210/endo-101-4-1325.
Intestinal calcium and phosphate transport was studied in normal and hypophosphatemic mice fed a variety of dietary regimens with and without vitamin D. Regardless of dietary phosphorus levels, the genetic hypophosphatemic mice had drastically reduced levels of serum inorganic phosphate and intestinal phosphate transport while showing only slightly reduced serum calcium and intestinal calcium transport levels. The inclusion of vitamin D in the diet did not increase the low serum phosphorus levels and low rates of intestinal phosphate transport in the genetic hypophosphatemic mice, while it did increase serum calcium and intestinal calcium transport levels. The administration of 1,25-dihydroxyvitamin D3 to the hypophosphatemic mice stimulated intestinal calcium transport but had no effect on intestinal phosphate transport. In contrast, the 1,25-dihydroxyvitamin D3 stimulated both phosphate and calcium transport in the intestine of normal mice. The results obtained are consistent with the hypothesis that the primary metabolic disturbance in familial hypophosphatemia involves a defect in phosphate transport mechanisms.
在喂食了各种含或不含维生素D饮食方案的正常小鼠和低磷血症小鼠中,对肠道钙和磷的转运进行了研究。无论饮食中的磷水平如何,遗传性低磷血症小鼠的血清无机磷水平和肠道磷转运水平都大幅降低,而血清钙和肠道钙转运水平仅略有降低。在遗传性低磷血症小鼠的饮食中添加维生素D并没有提高其低血清磷水平和低肠道磷转运率,而确实提高了血清钙和肠道钙转运水平。给低磷血症小鼠注射1,25 - 二羟基维生素D3可刺激肠道钙转运,但对肠道磷转运没有影响。相比之下,1,25 - 二羟基维生素D3刺激了正常小鼠肠道中的磷和钙转运。所得结果与家族性低磷血症的主要代谢紊乱涉及磷转运机制缺陷这一假设一致。