摘要
长期用重度缺碘地区食物饲养大鼠复制地方性克汀病动物模型,观察了第四、五代仔鼠20日龄时的实验结果。发现大脑核T_3受体最大结合容量(MBC)及受体提取液中内源T_3已明显下降,核内T_3减少极为显著,而T_45′-脱碘酶活性也同步下降,表明在大脑T_3不足时,核受体MBC减少可能是地方性克汀病发病的始动环节。
We observed the changes of cerebral nuclear T3 and its receptors and T4 5'-deiodinase activity in the fourth or fifth filial generations of the rats with long term iodine deficiency. The cerebrum was dissected on the 20th day postpartum. The results showed that the maximal binding capacity of nuclear T3 receptor was significantly lowered, but the affinity constant was essentially unchanged. Also, the concentration of nuclear T3 and the T4 5'-deiodinase activity were decreased markedly. It was concluded that 1) A decrease of cerebral nuclear T3 receptor was induced by long term iodine deficiency in rats; 2) T4 5'-deiodinase activity rather than serum T3 level could reflect more precisely the cerebral nuclear T3 concentration; and 3) The decrease of T3 receptor may presumably be the initial step of endemic cretinism caused by severe iodine deficiency.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
1991年第1期30-32,共3页
Chinese Journal of Endocrinology and Metabolism
关键词
碘缺乏
克汀病
核T3受体
地方性
Iodine deficiency Endemic cretinism Nuclear T3 receptor T45'-deiodinase