Insulin markedly potentiates the capacity of parathyroid hormone to increase expression of 25-hydroxyvitamin D3-24-hydroxylase in rat osteoblastic cells in the presence of 1,25-dihydroxyvitamin D3.
Insulin markedly potentiates the capacity of parathyroid hormone to increase expression of 25-hydroxyvitamin D3-24-hydroxylase in rat osteoblastic cells in the presence of 1,25-dihydroxyvitamin D3.
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在 1,25-二羟基维生素 D3 存在的情况下，胰岛素显着增强甲状旁腺激素增加大鼠成骨细胞中 25-羟基维生素 D3-24-羟化酶表达的能力。
DOI：
10.1016/0014-5793(96)00856-3
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发表时间：
1996
期刊：
影响因子：
3.5
通讯作者：
Wongsurawat,N
中科院分区：
文献类型：
--
作者：
Armbrecht,HJ;Wongsurawat,VJ;Hodam,TL;Wongsurawat,N
我们之前已经证明胰岛素会改变25-羟基维生素D的肾脏代谢。为了检查胰岛素对骨骼中维生素D代谢的影响，我们使用UMR-106成骨细胞样细胞来研究胰岛素对25(OH)D3-24-羟化酶(24-羟化酶)表达的调节。 24-羟化酶是降解靶组织中1,25-二羟基维生素D3(1,25(OH)2D)的重要酶。单独使用胰岛素对 UMR 细胞中 24-羟化酶的细胞色素 P450 成分 (CYP24) 的 mRNA 水平或 24-羟化酶活性本身没有影响。然而，在 1,25(OH)2D 存在的情况下，胰岛素可增强甲状旁腺激素 (PTH) 的能力，使 CYP24 mRNA 水平提高 3-4 倍，并将 24-羟化酶活性提高 2 倍。胰岛素增加了 UMR 细胞对 PTH 的最大反应性，但不改变其敏感性。胰岛素的作用需要 1,25(OH)2D 的存在，并且部分依赖于新蛋白质的合成。胰岛素样生长因子 1 也增强了 PTH 的作用。 PTH 和胰岛素对 24-羟化酶的这种显着刺激可能有助于调节 1,25(OH)2D 作用和/或在骨细胞中产生 24,25-二羟基维生素 D。
We have previously shown that insulin alters the renal metabolism of 25-hydroxyvitamin D. To examine the effect of insulin on vitamin D metabolism in bone, we have used UMR-106 osteoblast-like cells to study the regulation of 25(OH)D3-24-hydroxylase (24-hydroxylase) expression by insulin. The 24-hydroxylase is an important enzyme in degrading 1,25-dihydroxyvitamin D3(1,25(OH)2D) in target tissues. Insulin alone had no effect on mRNA levels of the cytochrome P450 component (CYP24) of the 24-hydroxylase or on 24-hydroxylase activity itself in UMR cells. However, insulin increased the capacity of parathyroid hormone (PTH) to elevate CYP24 mRNA levels by 3–4 fold and to increase 24-hydroxylase activity by 2-fold in the presence of 1,25(OH)2D. Insulin increased the maximal responsiveness of UMR cells to PTH without altering their sensitivity. The action of insulin required the presence of 1,25(OH)2D and was partly dependent on new protein synthesis. Insulin-like growth factor 1 also potentiated the effects of PTH. This marked stimulation of the 24-hydroxylase by PTH and insulin may serve to regulate 1,25(OH)2D action and/or to produce 24,25-dihydroxyvitamin D in bone cells.