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在男性胰岛素受体基质4淘汰赛小鼠中,下丘脑-垂体-甲状腺轴完好无损

Emilie Brûlé¹, Xiang Zhou², Ying Wang³

¹E Brûlé, Department of Anatomy and Cell Biology, McGill University, Montreal, Canada.

European thyroid journal

|January 25, 2024

概括

胰岛素受体基质4 (IRS4) 淘汰小鼠不会发展到中央甲状腺功能低下症. 这表明另一种IRS蛋白可能会补偿IRS4的损失,与人类的IRS4缺乏不同.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

胰岛素受体基质4 (IRS4) 基因的功能丧失突变会导致男性的X结合性先天性中央甲状腺功能低下症.
在信号通路中,IRS4 起到支架蛋白的作用,但其在甲状腺刺激激素 (TSH) 调节中的确切作用尚不清楚.

研究的目的:

研究IRS4在下丘脑-垂体-甲状腺轴中的作用.
为了确定IRS4淘汰赛小鼠是否模拟人类的IRS4缺乏.

主要方法:

产生了两个具有移突变的全球Irs4淘汰鼠标系.
评估了垂体TSH亚单元的基因表达,TRH受体和下丘脑Trh表达.
评估血清甲状腺激素水平 (T3,T4) 和TSH对诱导的甲状腺功能低下症的反应.

主要成果:

伊尔斯4淘汰赛的雄性表现出正常的垂体TSH亚单元基因表达和TRH受体水平.
血清甲状腺激素和下丘脑Thr表达在淘汰的小鼠中是正常的.
诱导的甲状腺功能低下症导致了类似的TSH增加在淘汰赛和野生型小鼠.

结论:

伊尔斯4淘汰赛小鼠没有表现出中央甲状腺功能低下症.
这些小鼠不能完全复制IRS4缺乏的患者.
其他IRS蛋白质的补偿可能解释了IRS4淘汰小鼠的euthyroid状态.

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