Dietary modification of thyroxine deiodination in rat liver is not mediated by hepatic sulfhydryls.
Dietary modification of thyroxine deiodination in rat liver is not mediated by hepatic sulfhydryls.
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大鼠肝脏中甲状腺素脱碘的饮食调整不是由肝巯基介导的。
DOI：
10.1172/jci109751
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
M. Moeller
中科院分区：
文献类型：
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作者：
L. Gavin;F. McMAHON;M. Moeller
甲状腺素（T（4））的酶促脱碘是巯基依赖性的。禁食（72小时）可抑制肝脏T（4）脱碘，并降低非蛋白巯基（NP-SH）和还原型谷胱甘肽（GSH）的肝脏含量。有人提出，禁食效应可能是通过肝巯基的这些变化介导的。为了检验组织（肝）巯基含量在饮食控制后T（4）脱碘修饰中的重要性，我们检测了T（4）向3，5，3 '-三碘甲腺原氨酸（T（3））的顺序脱碘。（5 '-脱碘）和3，3'，5-三碘甲状腺原氨酸（反向T（3），rT（3））来自饲喂Purina实验室食物的大鼠组的未添加硫醇的肝匀浆中的（5-脱碘）（P）（富含蛋白质的饮食）、单独葡萄糖（G）或葡萄糖加半胱氨酸（G（c））72小时或禁食（F）相同时间。将每个反应的初始速率与NP-SH和GSH的组织浓度进行比较。饮食控制引起肝脏T（4）到T（3）和rT（3）的脱碘和巯基含量的显着变化。各反应速率与肝NP-SH和GSH水平之间存在显著的分离。T（4）通过交替途径的脱碘率在G > P > F组显著高于（P < 0.01）.而P > F > G时，肝脏NP-SH和GSH含量均显著高于F（P < 0.05）。在对喂食G（c）的大鼠的组织进行分析时，进一步强调了这些参数之间缺乏相关性。尽管G（c）喂养后肝脏NP-SH和GSH明显增加（P < 0.01），但与仅喂葡萄糖的组相比，碘甲腺原氨酸脱碘没有改变。这些数据表明，饮食对肝脏中T（4）单脱碘的影响不是由巯基化合物组织水平的变化介导的，而是涉及脱碘酶浓度的改变。
The enzymatic deiodination of thyroxine (T(4)) is thiol dependent. Fasting (72 h) depresses hepatic T(4) deiodination and lowers the hepatic content of nonprotein sulfhydryls (NP-SH) and reduced glutathione (GSH). It has been proposed that the fasting effect may be mediated through these alterations in hepatic sulfhydryls. To test the importance of tissue (hepatic) thiol content in the modification of T(4) deiodination consequent to dietary manipulation, we examined the sequential deiodination of T(4) to 3,5,3'-triiodothyronine (T(3)) (5'-deiodination) and 3,3',5-triiodothyronine (reverse T(3), rT(3)) (5-deiodination) in liver homogenates without added thiol from groups of rats fed Purina lab chow (P) (a protein-rich diet), glucose alone (G), or glucose plus cysteine (G(c)) for 72 h or fasted (F) for the same period. The initial rate of each reaction was compared to the tissue concentrations of NP-SH and GSH. Dietary manipulation induced significant changes in hepatic deiodination of T(4) to T(3) and rT(3) and sulfhydryl content. There was a marked dissociation between the rate of each reaction and hepatic NP-SH and GSH levels. T(4) deiodination by the alternative pathways was significantly higher (P < 0.01) in G > P > F. In contrast both hepatic NP-SH and GSH concentrations were greater (P < 0.05) in P > F > G. The lack of a relationship between these parameters was further emphasized on analysis of tissue from rats fed G(c). Despite the clearcut (P < 0.01) increase in hepatic NP-SH and GSH consequent to G(c) feeding, there was no alteration in iodothyronine deiodination compared to the group fed glucose alone. These data indicate that the effects of diet on T(4) monodeiodination in liver are not mediated by changes in the tissue level of sulfhydryl compounds but rather involve alterations in the concentrations of the deiodinases.