The contribution of local tissue thyroxine monodeiodination to the nuclear 3,5,3'-triiodothyronine in pituitary, liver, and kidney of euthyroid rats.
The contribution of local tissue thyroxine monodeiodination to the nuclear 3,5,3'-triiodothyronine in pituitary, liver, and kidney of euthyroid rats.
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DOI：
10.1210/endo-103-4-1196
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发表时间：
1978-10
期刊：
影响因子：
4.8
通讯作者：
J. E. Silva;T. Dick;P. Larsen
中科院分区：
文献类型：
--
作者：
J. E. Silva;T. Dick;P. Larsen
在甲状腺功能正常的大鼠中，测定了局部T4单脱碘和血浆T3对垂体前叶、肝脏和肾脏核T3的贡献。注射[125 I]T4后，血浆[125 I]T3的量逐渐增加，超过注射的污染物，在注射后约12 h达到峰值，此后血浆[125 I]T4的分数保持不变（2.8 × 10 - 3）。在垂体前叶组织的核中，局部产生的[125 I]T3也缓慢增加（超过血浆[125 I]T3），在[125 I]T4给药后约16 h达到峰值。注射T4后18和24小时，细胞内产生的细胞核[125 I] T3与血浆[125 I]T4的比值保持不变，垂体核为13 +/- 2 × 10 - 3，肝脏为2.0 +/- 0.4 × 10 - 3，肾脏为0.47 +/- 0.1 × 10 - 3（所有值均为平均值+/- SD）。在相同动物中，局部产生的T3导致[125 I]T3的核与血浆（N：P）比明显高于注射[131 I]T3。在垂体、肝脏和肾脏中，注射T4后平衡时[125 I]T3的N：P比分别为2.4 +/- 0.6、0.47 +/- 0.09和0.10 +/- 0.03（纳克T3（mg DNA）-1/ng T3 ml-1）。[131 I]T3 N：P比值的可比值为0.47 +/- 0.14（垂体）、0.18 +/- 0.01（肝脏）和0.036 +/- 0.008（肾脏）。使用RIA值的血浆T4和T3浓度在这些大鼠和最大核T3结合能力估计在平行实验中，来自血浆T3和从本地T4到T3单脱碘的核T3的重量的数量进行了估计，并表示为T3受体的饱和度的百分比。78%的核T3受体的网站在垂体前叶被占领的一半的核T3直接来自血浆T3和另一半来自垂体内T4单脱碘。局部T4单脱碘仅分别提供肝和肾细胞核T3的28%和14%，这些组织的核受体约为50%饱和。由于我们以前的研究表明，垂体核T3受体的占用可能会调节TSH的释放，这些数据提供了一种机制，通过这种机制，TSH分泌可能会改变血浆T3或T4的变化，而在肝脏和肾脏的核T3主要是血浆T3浓度的函数。
The contributions of local T4 monodeiodination and plasma T3 to the nuclear T3 of anterior pituitary, liver, and kidney were measured in euthyroid rats. After injection of [125I]T4, there was a gradual increase in the quantity of plasma [125I]T3 in excess of injected contaminant, which peaked at approximately 12 h after injection and remained a constant fraction of plasma [125I]T4 (2.8 X 10(-3) after that time. In the nuclei of anterior pituitary tissue, there was also a slow increase in locally produced [125I]T3 (in excess of that which could be accounted for by plasma [125I]T3) which appeared to peak at about 16 h after [125I]T4 administration. The ratio of nuclear [125I]T3 generated intracellularly to plasma [125I]T4 was constant at 18 and 24 h after T4 injection and was 13 +/- 2 X 10(-3) in nuclei of pituitary, 2.0 +/- 0.4 x 10(-3) in liver, and 0.47 +/- 0.1 x 10(-3) in kidney (all values are mean +/- SD). This locally generated T3 resulted in a markedly higher nuclear to plasma (N:P) ratio for [125I]T3 than for injected [131I]T3 in the same animals. The N:P ratio for [125I]T3 at equilibrium after injected T4 was 2.4 +/- 0.6, 0.47 +/- 0.09, and 0.10 +/- 0.03 (nanograms of T3 (mg DNA)-1/ng T3 ml-1) in pituitary, liver, and kidney. Comparable values for [131I]T3 N:P ratios were 0.47 +/- 0.14 (pituitary), 0.18 +/- 0.01 (liver), and 0.036 +/- 0.008 (kidney). Using RIA values for plasma T4 and T3 concentrations in these rats and maximal nuclear T3-binding capacities estimated in parallel experiments, the gravimetric quantities of nuclear T3 derived from plasma T3 and from local T4 to T3 monodeiodination were estimated and expressed as the percentage of saturation of T3 receptors. Seventy-eight percent of nuclear T3 receptor sites in anterior pituitary were occupied with one-half of the nuclear T3 derived directly from plasma T3 and the other half from intrapituitary T4 monodeiodination. Local T4 monodeiodination provided only 28% and 14%, respectively, of the nuclear T3 in liver and kidney, and the nuclear receptors of these tissues were about 50% saturated. Since our previous studies have shown that the occupancy of the pituitary nuclear T3 receptors may regulate TSH release, these data provide a mechanism by which TSH secretion could be altered by changes in either plasma T3 or T4, whereas nuclear T3 in liver and kidney is predominantly a function of the plasma T3 concentration.