Bjørn-Hansen Gøtzsche L S, Gøtzsche O, Flyvbjerg A, Boye N
Second University Clinic of Internal Medicine, Kommunehospitalet, Aarhus, Denmark.
Acta Endocrinol (Copenh). 1990 Jul;123(1):67-71. doi: 10.1530/acta.0.1230067.
In order to elucidate the day-by-day development of low T3 syndrome, we made rats diabetic by an injection of streptozotocin. Untreated controls killed at day 0 and rats treated for 8 days with insulin after they had received streptozotocin served as controls. Sub-groups of animals were killed 1, 2, 3, 4 and 8 days after streptozotocin. In serum, heart and liver, T3 was depressed to less than 50% of controls at day 4, whereas the insulin-treated rats differed from controls only as to heart T3. Heart iodothyronine 5'-deiodinase activity was depressed to a minimum at day 3 and depression was not prevented by insulin. Liver iodothyronine 5'-deiodinase activity had not reached a minimum at day 8, and again, insulin treatment did not normalize this parameter. T3 contents and iodothyronine 5'-deiodinase activity in brown adipose tissue did not differ from values in controls at any point of time. Thus, in the rats with low T3 syndrome induced by streptozotocin-diabetes, a lowered iodothyronine 5'-deiodinase activity is not fully inhibited by insulin treatment, whereas the T3 content in the liver is re-established during an observation period of 8 days. A direct toxic effect of streptozotocin seems unlikely as an in vitro study showed no influence of streptozotocin on iodothyronine 5'-deiodinase activity in the liver. The study thus indicates that iodothyronine 5'-deiodinase activity in the heart and liver is depressed in experimental diabetes, despite near optimal regulation of blood glucose, and we suggest that lowered intracellular T3 production could, after some time, result in a hypothyroid state in different tissues.
为了阐明低T3综合征的逐日发展情况，我们通过注射链脲佐菌素使大鼠患糖尿病。在第0天处死未治疗的对照大鼠，并将注射链脲佐菌素后用胰岛素治疗8天的大鼠作为对照。在注射链脲佐菌素后的第1、2、3、4和8天处死动物亚组。在血清、心脏和肝脏中，第4天时T3降至对照组的50%以下，而胰岛素治疗的大鼠仅在心脏T3方面与对照组不同。心脏碘甲腺原氨酸5'-脱碘酶活性在第3天降至最低，且胰岛素不能阻止其降低。肝脏碘甲腺原氨酸5'-脱碘酶活性在第8天尚未降至最低，同样，胰岛素治疗也未使该参数恢复正常。棕色脂肪组织中的T3含量和碘甲腺原氨酸5'-脱碘酶活性在任何时间点均与对照组的值无差异。因此，在由链脲佐菌素诱导的糖尿病低T3综合征大鼠中，胰岛素治疗不能完全抑制碘甲腺原氨酸5'-脱碘酶活性的降低，而肝脏中的T3含量在8天的观察期内得以恢复。链脲佐菌素的直接毒性作用似乎不太可能，因为一项体外研究表明链脲佐菌素对肝脏中的碘甲腺原氨酸5'-脱碘酶活性没有影响。该研究因此表明，在实验性糖尿病中，尽管血糖得到了近乎最佳的调节，但心脏和肝脏中的碘甲腺原氨酸5'-脱碘酶活性仍会降低，并且我们认为细胞内T3生成的降低在一段时间后可能会导致不同组织出现甲状腺功能减退状态。
