Deficiency of vitamin D metabolites directly stimulates renal 25-hydroxyvitamin D3-1-hydroxylase activity in rats.
Deficiency of vitamin D metabolites directly stimulates renal 25-hydroxyvitamin D3-1-hydroxylase activity in rats.
复制标题
维生素 D 代谢物缺乏会直接刺激大鼠肾脏 25-羟基维生素 D3-1-羟化酶活性。
DOI：
10.1016/0026-0495(91)90157-r
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Walters,MR
中科院分区：
文献类型：
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作者：
Fox,J;Kollenkirchen,U;Walters,MR
已知甲状旁腺激素（PTH）、低磷酸盐血症和低钙血症会增加大鼠肾脏25-羟基维生素D3-1-羟化酶（1-羟化酶）的酶活性。因此，酶活性在维生素D缺乏状态下显著增加，但这种刺激是否是对维生素D缺乏的直接反应，或仅在血浆钙、磷酸盐或PTH的相关变化后发生尚不清楚。我们测试是否维生素D缺乏本身影响1-羟化酶活性的肾皮质切片使用正常钙的大鼠模型维生素D缺乏症。断奶雄性大鼠喂食以下三种饮食之一：（A）0.8% Ca，0.5% P，2.2 IU维生素D3/g;或维生素D缺乏饮食，（B）0.8% Ca，0.5% P;和（C）2.0% Ca，1.25% P，20%乳糖。维生素D缺乏的大鼠喂食饲料B在两个测试期间都出现低钙血症，PTH升高，与喂食饲料A的大鼠相比，1-羟化酶活性增加100倍以上。A组和C组的血浆钙、磷酸盐和PTH水平相同，但与A组大鼠相比，C组的1-羟化酶活性也显著升高（10周和19周饮食后分别增加104倍和17倍）。这些数据导致的重要结论，严重缺乏维生素D代谢物本身提供了一个强大的和独立的刺激肾1-羟化酶活性的大鼠，可能是由于缺乏1，25（OH）2D 3介导的酶抑制。
Renal 25-hydroxyvitamin D3-1-hydroxylase (1-hydroxylase) enzyme activity in rats is known to be increased by parathyroid hormone (PTH), hypophosphatemia, and hypocalcemia. Thus, enzyme activity is markedly increased in vitamin D-deficient states, but whether this stimulation is a direct response to the vitamin D deficiency or only occurs following the associated changes in plasma calcium, phosphate, or PTH is unclear. We tested whether vitamin D deficiency per se influences 1-hydroxylase activity in renal cortical slices using a normocalcemic rat model of vitamin D deficiency. Weanling male rats were fed one of the following three diets: (A) 0.8% Ca, 0.5% P, 2.2 IU vitamin D3/g; or vitamin D-deficient diets containing, (B) 0.8% Ca, 0.5% P; and (C) 2.0% Ca, 1.25% P, 20% lactose. Vitamin D-deficient rats fed diet B were hypocalcemic with elevated PTH at both test periods, and 1-hydroxylase activity was increased more than 100-fold compared with rats fed diet A. Plasma calcium, phosphate, and PTH levels were the same in groups A and C, but 1-hydroxylase activity was also substantially elevated in group C versus group A rats (104- and 17-fold increases after 10 and 19 diet weeks, respectively). These data lead to the important conclusion that severe deficiency of vitamin D metabolites per se provides a strong and independent stimulus to renal 1-hydroxylase activity in rats, perhaps due to the absence of 1,25(OH)2D3-mediated enzyme inhibition.