首页> 美国卫生研究院文献>Endocrinology >Mice With Hepatocyte-Specific Deficiency of Type 3 Deiodinase Have Intact Liver Regeneration and Accelerated Recovery From Nonthyroidal Illness After Toxin-Induced Hepatonecrosis
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Mice With Hepatocyte-Specific Deficiency of Type 3 Deiodinase Have Intact Liver Regeneration and Accelerated Recovery From Nonthyroidal Illness After Toxin-Induced Hepatonecrosis

机译:具有肝细胞特异性缺陷的3型脱碘酶的小鼠在毒素诱导的肝坏死后具有完整的肝再生和非甲状腺疾病的加速恢复

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摘要

Type 3 deiodinase (D3), the physiologic inactivator of thyroid hormones, is induced during tissue injury and regeneration. This has led to the hypotheses that D3 impacts injury tolerance by reducing local T3 signaling and contributes to the fall in serum triiodothyronine (T3) observed in up to 75% of sick patients (termed the low T3 syndrome). Here we show that a novel mutant mouse with hepatocyte-specific D3 deficiency has normal local responses to toxin-induced hepatonecrosis, including normal degrees of tissue necrosis and intact regeneration, but accelerated systemic recovery from illness-induced hypothyroxinemia and hypotriiodothyroninemia, demonstrating that peripheral D3 expression is a key modulator of the low T3 syndrome.
机译:3型脱碘酶(D3)是甲状腺激素的生理失活剂,在组织损伤和再生过程中被诱导。这导致了这样的假设,即D3通过减少局部T3信号传导来影响损伤耐受性,并导致在多达75%的患病患者(称为低T3综合征)中观察到的血清三碘甲状腺素(T3)下降。在这里,我们显示具有肝细胞特异性D3缺乏症的新型突变小鼠对毒素诱导的肝坏死具有正常的局部反应,包括正常程度的组织坏死和完整的再生,但是从疾病引起的甲状腺功能低下血症和甲状腺功能低下的甲状腺激素血症加速了系统性恢复,表明外周血D3表达是低T3综合征的关键调节因子。

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