Regulation of rat thyroxine-binding globulin and transthyretin: studies in thyroidectomized and hypophysectomized rats given tri-iodothyronine or/and growth hormone.
Regulation of rat thyroxine-binding globulin and transthyretin: studies in thyroidectomized and hypophysectomized rats given tri-iodothyronine or/and growth hormone.
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DOI：
10.1677/joe.0.1420077
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发表时间：
1994-07
期刊：
影响因子：
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通讯作者：
R. Vranckx;M. Rouaze-Romet;L. Savu;P. Méchighel;M. Maya;Emmanuel A. Nunez
中科院分区：
文献类型：
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作者：
R. Vranckx;M. Rouaze-Romet;L. Savu;P. Méchighel;M. Maya;Emmanuel A. Nunez
我们研究了甲状腺与垂体在调节大鼠血清中两种可饱和甲状腺激素载体甲状腺素结合球蛋白（TBG）和甲状腺素运载蛋白（TTR）中的作用。我们研究了，在血清和肝脏mRNA水平，TBG和TTR甲状腺切除术（Tx），垂体切除术（Hx）和替代治疗与三碘甲状腺原氨酸（T3）或/和GH，这两种激素被耗尽时，甲状腺或垂体被删除。这些研究是在8周龄的雄性大鼠上进行的，此时发育调节的TBG在其短暂的出生后升高后变得不可检测，而非发育调节的TTR呈现其正常的、与年龄无关的表达水平。Tx诱导的TBG再表达被T3替代完全逆转，并且对GH替代无反应。TTR在血清中，另一方面，不受Tx或T3替代，中度减少Tx的mRNA的量，并显着减少GH替代。此外，GH治疗抑制甲状腺功能正常对照组TTR的表达。Hx，像Tx，诱导TBG重新表达，T3替代有效拮抗的效果。然而，TBG合成Hx高于Tx大鼠和有效拮抗T3替代。最出乎意料的是，GH诱导TBG合成的显著进一步增加，并且GH替代的Hx大鼠中合成的TBG完全抵抗T3替代的下调。TTR在血清和肝脏水平均显著降低，不受T3的影响，并进一步降低GH替代。（250字处删节）
We have investigated the role of the thyroid compared with the hypophysis in the regulation of the two saturable thyroid hormone carriers of rat serum, thyroxine-binding globulin (TBG) and transthyretin (TTR). We examined, at serum and hepatic mRNA level, the responses of TBG and TTR to thyroidectomy (Tx), hypophysectomy (Hx) and replacement treatments with tri-iodothyronine (T3) or/and GH, both hormones which are depleted when the thyroid or hypophysis are removed. The studies were performed on male rats at the age of 8 weeks, when the developmentally regulated TBG becomes undetectable after its transient postnatal rise, while the nondevelopmentally regulated TTR presents its normal, age-independent level of expression. Tx-induced TBG re-expression was completely reversed by T3 replacement and unresponsive to GH replacement. TTR in the serum, on the other hand, was not affected by Tx or T3 replacement, moderately reduced by Tx in terms of the amount of mRNA, and markedly reduced by GH replacement. GH treatment, moreover, inhibited the expression of TTR in euthyroid controls. Hx, like Tx, induced TBG re-expression, an effect efficiently antagonized by T3 replacement. However, TBG synthesis was higher in Hx than in Tx rats and less effectively antagonized by T3 replacement. Most unexpectedly, GH induced a dramatic further increase in TBG synthesis, and the TBG synthesized in the GH-replaced Hx rats was entirely resistant to down-regulation by T3 replacement. TTR was markedly decreased at both serum and hepatic levels by Hx, unaffected by T3 and further decreased by GH replacement.(ABSTRACT TRUNCATED AT 250 WORDS)