Gafni M, Saddok C, Sirkis N, Gross J
Endocrinology. 1977 Apr;100(4):1186-91. doi: 10.1210/endo-100-4-1186.
The time course of the effect of bovine TSH (bTSH) on serum concentrations of thyroxine (T4) and triiodothyronine (T3) was measured in the normal mouse. The basal, unstimulated levels were 3.2+/-1.1 mug/100 ml T4 and 104+/-25 ng/100 ml T3 (mean+/-SD). With doses of bTSH from 0.5 to 100 mU the peak levels of the thyroid hormones were only 2.6 and 1.8 times the basal level for T4 and T3, respectively. With increasing doses of bTSH there was a proportional prolongation of the increased serum levels of thyroid hormones, i.e., about 2 h for 0.5mU to 12 h for 100 mU TSH. The integrated response with time was linearly related to the log dose. This would suggest a control mechanism which prevents excessive concentration of thyroid hormones in the serum. This pattern of response to TSH differs somewhat from that obtained by following radioiodine release in the McKenzie type bio-assay. To avoid the problems of changing blood concentrations of thyroid hormones and TSH, the release of T4 and T3 from the mouse thyroid was measured in vitro. The secretion increased with bTSH concentrations in the range of 0.02-0.8 mU/ml for T4 and 0.02-0.4 mU/ml for T3. The maximal response was 8.8+/-0.5 ng T4/3h/thyroid and 3.6+/-0.3 ng T3/3h/thyroid as against the basal secretion of 2.4+/-0.2ng T4 and 0.8+/-0.1 ng T3 (mean+/-SEM). Further in crease in bTSH concentration was associated with a decreased rate of thyroid hormone release. Thyroidal cAMP accumulation was enhanced with increasing bTSH concentration, even when there was a decrease in secretion. The dichotomy in the dose-response pattern between the two parameters indicated that the effect of high TSH concentrations on the release was induced at a step beyond cAMP accumulation. This was corroborated by the similar pattern of release induced by increasing concentration of DBcAMP. These findings indicate the existence of an intrathyroidal autoregulatory mechanism which prevents excess increase of thyroid hormone levels in the blood.
在正常小鼠中测量了牛促甲状腺激素（bTSH）对血清甲状腺素（T4）和三碘甲状腺原氨酸（T3）浓度影响的时间进程。基础的、未受刺激的水平分别为3.2±1.1μg/100ml T4和104±25ng/100ml T3（均值±标准差）。给予0.5至100mU剂量的bTSH时，甲状腺激素的峰值水平分别仅为T4和T3基础水平的2.6倍和1.8倍。随着bTSH剂量增加，血清甲状腺激素水平升高的持续时间成比例延长，即0.5mU时约为2小时，100mU TSH时为12小时。随时间的综合反应与对数剂量呈线性相关。这表明存在一种控制机制，可防止血清中甲状腺激素过度浓缩。这种对TSH的反应模式与在麦肯齐型生物测定中追踪放射性碘释放所获得的模式有所不同。为避免甲状腺激素和TSH血浓度变化的问题，在体外测量了小鼠甲状腺中T4和T3的释放。对于T4，分泌随bTSH浓度在0.02 - 0.8mU/ml范围内增加，对于T3，在0.02 - 0.4mU/ml范围内增加。最大反应分别为8.8±0.5ng T4/3h/甲状腺和3.6±0.3ng T3/3h/甲状腺，而基础分泌分别为2.4±0.2ng T4和0.8±0.1ng T3（均值±标准误）。bTSH浓度进一步升高与甲状腺激素释放速率降低相关。即使分泌减少，甲状腺cAMP积累也随bTSH浓度增加而增强。两个参数剂量 - 反应模式的二分法表明，高TSH浓度对释放的影响是在cAMP积累之外的一个步骤诱导的。增加DBcAMP浓度诱导的类似释放模式证实了这一点。这些发现表明存在一种甲状腺内自动调节机制，可防止血液中甲状腺激素水平过度升高。
