EXPERIMENTAL DIABETES IN THE RAT CAUSES AN INSULIN-REVERSIBLE DECREASE IN RENAL 25-HYDROXYVITAMIN-D3-1ALPHA-HYDROXYLASE ACTIVITY
EXPERIMENTAL DIABETES IN THE RAT CAUSES AN INSULIN-REVERSIBLE DECREASE IN RENAL 25-HYDROXYVITAMIN-D3-1ALPHA-HYDROXYLASE ACTIVITY
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DOI：
10.1210/endo-107-1-300
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发表时间：
1980-01-01
期刊：
影响因子：
4.8
通讯作者：
TOBIASSEN, O
中科院分区：
文献类型：
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作者：
MARTIN, E;KHALIL, SM;TOBIASSEN, O
糖尿病大鼠肠黏膜对钙的吸收减少是由于低循环1,25-二羟基维生素D3 [1,25-(OH)2D3]水平。研究了血浆1,25-(OH)2D3降低的原因，以及糖尿病患者肠道黏膜中1,25-(OH)2D3掺入可能存在缺陷的可能性。在糖尿病大鼠中，i.v [3H]1,25-(OH)2D3的代谢清除率没有增加，提示其血浆中1,25-(OH)2D3水平低是由于形成减少所致。标准剂量[3H]25-羟基维生素D3 （[3H]25- ohd3）在糖尿病大鼠体内转化为[3H]1,25-(OH)2D3减少了60%；胰岛素治疗后恢复正常。血清钙和磷水平不受糖尿病的影响。由于糖尿病不增加1,25-(OH)2D3的分解代谢，[3H]25OHD3转化为[3H]1,25-(OH)2D3的减少表明肾脏25-OH- d3 -1 - α的活性。糖尿病大鼠-羟化酶降低。糖尿病大鼠肠黏膜明显肥大。[3H]1,25-(OH)2D3的掺入没有内在缺陷，糖尿病大鼠肠道钙吸收的下降显然是由于肾1 α降低导致1,25-(OH)2D3向肠黏膜的递送减少。羟化酶的活动。是否减少了1。-羟化酶活性是由于胰岛素缺乏还是糖尿病状态的继发性后果尚不清楚。
The decreased intestinal mucosal absorption of Ca observed in the diabetic rat was attributed to low circulating 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] levels. The cause of the depressed plasma 1,25-(OH)2D3 and the possibility that in diabetes the incorporation of 1,25-(OH)2D3 into intestinal mucosa may be defective were investigated. In diabetic rats, the metabolic clearance of i.v. [3H]1,25-(OH)2D3 was not increased, suggesting that their low plasma 1,25-(OH)2D3 levels were due to decreased formation. The in vivo conversion of a standard dose of [3H]25-hydroxyvitamin D3 ([3H]25-OHD3) to [3H]1,25-(OH)2D3 was reduced by 60% in diabetic rats; it returned to normal by insulin treatment. Serum Ca and P levels were unaffected by diabetes. Since diabetes did not augment 1,25-(OH)2D3 catabolism, the decreased conversion of [3H]25OHD3 to [3H]1,25-(OH)2D3 indicates that the activity of the renal 25-OH-D3-1.alpha.-hydroxylase is decreased in diabetic rats. Intestinal mucosa of diabetic rats was significantly hypertrophied. There was no intrinsic defect in the incorporation of [3H]1,25-(OH)2D3 The depressed intestinal Ca absorption in diabetic rats apparently is due to decreased delivery of 1,25-(OH)2D3 to the intestinal mucosa consequent to decreased renal 1.alpha.-hydroxylase activity. Whether the decrease in 1.alpha.-hydroxylase activity is due to insulin deficiency or is a secondary consequence of the diabetic state is unknown.