Renal parathyroid hormone-dependent adenylate cyclase activity after repletion of vitamin D-deficient rats with vitamin D-2.
Renal parathyroid hormone-dependent adenylate cyclase activity after repletion of vitamin D-deficient rats with vitamin D-2.
复制标题
维生素 D 缺乏大鼠补充维生素 D-2 后肾甲状旁腺激素依赖性腺苷酸环化酶活性。
DOI：
10.1016/0304-4165(80)90160-9
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
L. R. Forte
中科院分区：
文献类型：
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作者：
David L. Carnes;C. S. Anast;L. R. Forte
大鼠喂养的饮食缺乏维生素D和Ca 2+表现出更大的抑郁症的肾甲状旁腺激素（PTH）依赖性腺苷酸环化酶比观察到的大鼠喂养的饮食缺乏维生素D或钙。血清总Ca 2+从对照水平11.2 mg/dl降低到仅喂食钙缺乏饮食的大鼠的8.5 mg/dl，在喂食维生素D缺乏饮食的大鼠中降低到5.4 mg/dl。在维生素D和Ca 2+缺乏的饮食中，大鼠的血清钙进一步降低至4.3 mg/dl。血清免疫反应性PTH显着升高超过对照水平时，大鼠喂食试验饮食，但是，有三个实验组的升高水平之间没有显着差异。维生素D缺乏的大鼠仅用3200 I.U.的单次口服剂量进行补充。维生素D-2导致血清钙恢复到正常水平，血清PTH恢复到对照状态，并且PTH依赖性腺苷酸环化酶活性相关增加到72小时的对照水平。用相同剂量的维生素D-2补充缺乏维生素D和Ca 2+的大鼠，72 h后血清Ca 2+升高至7.2 mg/dl，但并未导致循环PTH减少，也未导致膜腺苷酸环化酶对PTH的反应性有任何显着改善。这些结果表明，甲状旁腺素升高是一个因素，在下调的甲状旁腺素依赖性腺苷酸环化酶，但不排除钙作为一个调节因子的作用。
Rats fed a diet deficient in both vitamin D and Ca2+exhibited a greater depression of the renal parathyroid hormone (PTH)-dependent adenylate cyclase than was observed in rats fed diets deficient in either vitamin D or calcium. Total serum Ca2+was decreased from a control level of 11.2 mg/dl to 8.5 mg/dl in rats fed the diet deficient in calcium alone, and to 5.4 mg/dl in rats fed the diet deficient in vitamin D. Serum calcium was decreased further to 4.3 mg/dl in rats fed the diet deficient in both vitamin D and Ca2+. Serum immunoreactive PTH was significantly elevated over control levels when rats were fed the test diets; however, there were no significant differences between the elevated levels in the three experimental groups. Repletion of rats deficient in vitamin D only with a single oral dose of 3200 I.U. vitamin D-2 resulted in restoration of serum calcium to normal levels, a return of serum PTH to the control state, and an associated increase in PTH-dependent adenylate cyclase activity to the control level by 72 h. Repletion of rats deficient in both vitamin D and Ca2+with the same dose of vitamin D-2 raised serum Ca2+to 7.2 mg/dl by 72 h, but did not cause a reduction in circulating PTH, nor did it result in any significant improvement in the responsiveness of the membrane adenylate cyclase to PTH. These results suggest that elevated PTH is a factor in the down regulation of the PTH-dependent adenylate cyclase, but do not rule out a role for calcium as a regulatory factor.