Fukuda H, Yasuda N, Greer M A, Kutas M, Greer S E
Endocrinology. 1975 Aug;97(2):307-14. doi: 10.1210/endo-97-2-307.
We have measured plasma thyroxine (T4), triiodothyronine (T3), and TSH with specific radioimmunoassays in rats during adaptation to severe iodine deficiency after they had previously received regimens supplying various quantities of iodine. Rats were maintained on a high-iodine diet (HID) containing 3 mg iodine/kg or a low-iodine diet (LID) containing 30 mug iodine/kg supplemented with 0.1, 0.2, or 0.4 mug iodine/ml of drinking water before swtiching to KID alone. Frequent serial blood samples were obtained up to 3 months, using 6 or more animals for each time interval. In animals originally fed HID, T4 remained at 4-6 mug/100 ml unitl the tenth day of LID, then rapidly decreased to a value of less than 0.4 mug/100 ml at 1 month. TSH was initially 50 muU/ml and increased linearly to 165 muU/ml on day 16. Thence there was a much more rapid rate of rise to 640 muU/ml at 38 days. The rats changed to LID alone after having been fed LID with iodine supplementation underwent similar qualitative hormonal changes. However, the decrease in plasma T4 and the increase in plasma TSH occurred sooner in the rats which had drunk water containing only 0.1 or 0.2 mug iodine/ml than in the previous experiment. Rats which had received 0.4 mug iodine/ml showed a pattern essentially identical to that of the animals which had been fed HID. plasma T3 did not change significantly in any of the experiments, remaining at 60-90 ng/100 ml, although there was a tendency for the values to be somewhat lower after several weeks of LID. There was a highly significant negative correlation of plasma T4 with plasma TSH. There was no significant correlation of plasma T3 with either plasma T4 or plasma TSH. It is concluded that the combined physiologic effect of plasma T4 and T3 concentration is more important in determining TSH secretion through negative feedback effects on the hypothalamus and/or pituitary than is the concentration of plasma T3.
我们采用特异性放射免疫分析法,对先前接受过不同碘摄入量方案的大鼠在适应严重碘缺乏过程中的血浆甲状腺素(T4)、三碘甲状腺原氨酸(T3)和促甲状腺激素(TSH)进行了测定。在单独切换到无碘饮食(KID)之前,大鼠分别维持在含3毫克碘/千克的高碘饮食(HID)或含30微克碘/千克的低碘饮食(LID)中,并分别补充0.1、0.2或0.4微克碘/毫升的饮用水。在长达3个月的时间内频繁采集系列血样,每个时间间隔使用6只或更多动物。在最初喂食HID的动物中,T4在LID的第10天之前一直保持在4 - 6微克/100毫升,然后在1个月时迅速降至低于0.4微克/100毫升。TSH最初为50微单位/毫升,在第16天线性增加至165微单位/毫升。此后,在第38天迅速上升至640微单位/毫升。在喂食补充碘的LID后再单独切换到LID的大鼠中,也出现了类似的激素定性变化。然而,饮用仅含0.1或0.2微克碘/毫升水的大鼠,其血浆T4的降低和血浆TSH的增加比之前的实验发生得更早。接受0.4微克碘/毫升的大鼠表现出与喂食HID的动物基本相同的模式。在任何实验中,血浆T3均无显著变化,维持在60 - 90纳克/100毫升,尽管在LID几周后其值有略低的趋势。血浆T4与血浆TSH呈高度显著的负相关。血浆T3与血浆T4或血浆TSH均无显著相关性。得出的结论是,血浆T4和T3浓度的联合生理效应,通过对下丘脑和/或垂体的负反馈作用来决定TSH分泌,比血浆T3浓度更为重要。