Shishiba Y, Takaishi M, Miyachi Y, Ozawa Y
Endocrinol Jpn. 1975 Aug;22(4):367-71. doi: 10.1507/endocrj1954.22.367.
In order to examine the hypothesis that the thyroidal responsiveness to TSH is under the influence of thyroid hormone, following the T3 injection to the mice, serum T3 concentrations and the response of thyroid tissue to a fixed dose of TSH in terms of intracellular colloid droplet formation was studied. The colloid droplets induced by TSH was significantly reduced when serum T3 was decreasing, while it was significantly increased when serum T3 was increasing. This results demonstrate for the first time the existence of short feed-back loop regulating intra-thyroidal function by circulating T3. To delineate the possible mechanism of action of T3, the thyroid gland of mouse whose serum T3 concentration was elevated by injecting 50 mug T3, was incubated with TSH in vitro. TSH-induced cyclic AMP generation was not inhibited at all but colloid droplet formation was significantly inhibited in the thyroid tissue of the animal whose serum T3 concentration was enormously high. Thus, it was demonstrated that the site at which T3 affects is beyond cylcic AMP generation but prior to endocytosis, being consistent with our previous results.
为了检验甲状腺对促甲状腺激素（TSH）的反应性受甲状腺激素影响这一假说，给小鼠注射三碘甲状腺原氨酸（T3）后，研究了血清T3浓度以及甲状腺组织对固定剂量TSH的反应（以细胞内胶体小滴形成为指标）。当血清T3下降时，TSH诱导的胶体小滴显著减少，而当血清T3上升时则显著增加。这一结果首次证明了存在由循环T3调节甲状腺内功能的短反馈环。为了阐明T3可能的作用机制，将通过注射50微克T3使血清T3浓度升高的小鼠甲状腺在体外与TSH一起孵育。TSH诱导的环磷酸腺苷（cAMP）生成完全未受抑制，但在血清T3浓度极高的动物的甲状腺组织中，胶体小滴形成受到显著抑制。因此，证明了T3作用的位点在cAMP生成之后但在内吞作用之前，这与我们之前的结果一致。
