HUMAN RECOMBINANT INTERLEUKIN-1-BETA DECREASES PLASMA THYROID-HORMONE AND THYROID STIMULATING HORMONE LEVELS IN RATS
HUMAN RECOMBINANT INTERLEUKIN-1-BETA DECREASES PLASMA THYROID-HORMONE AND THYROID STIMULATING HORMONE LEVELS IN RATS
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DOI：
10.1210/endo-123-5-2175
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发表时间：
1988-11-01
期刊：
影响因子：
4.8
通讯作者：
BURGER, AG
中科院分区：
文献类型：
--
作者：
DUBUIS, JM;DAYER, JM;BURGER, AG
在用单次注射人重组白细胞介素-1 β sc处理的大鼠中研究甲状腺功能。（hrIL-1）。在5小时内，12.5 μ g hr IL-1使总血清T4水平降低30 ± 10%。血清T_3水平降低35 ± 1.2%（P < 0.01）。4%（P < 0.001）。然而，游离T4和T3组分在前140分钟内显著增加162 ± 1.5%。20%（P < 0.001）和55 ± 0.5%（P <0.01）。4%（P < 0.001），导致88 . ±.游离T4浓度增加20%（P < 0.001），但游离T3浓度未增加。在hrIL-1注射后5小时，血清TSH浓度下降77 ± 0.01。3%（P < 0.001）。用0.125 μ g hrIL-1观察到类似的降低。5小时的饥饿没有改变血清TSH水平，这表明hrIL-1对TSH的影响不是由于减少食物摄入。为了测试血清TSH的降低是否是由于垂体内T3的增加，在甲状腺功能减退的大鼠中注射hrIL-1：血清TSH的下降没有被阻止，并且它在5小时内从14.05 ±. 0.56至9.66 ±。0.98 ng/ml（31%，P < 0.01，n = 14）。这些结果表明，hrIL-1的作用独立于甲状腺激素。通过在数天内植入[125]T4分泌微型泵来研究T4的外周代谢。对照组和给药组动物之间的T4血浆清除率无差异。因此，血清T4的下降是由分泌减少而不是由增加cataline解释的，因为无法检测到T4的连接裂解和肝脱碘酶的变化。因此，我们认为hrIL-1抑制甲状腺功能主要在下丘脑-垂体水平。
Thyroid function was investigated in rats treated sc with a single injection of human recombinant interleukin-1.beta. (hrIL-1). In 5 h 12.5 .mu.g hrIL-1 decreased total serum T4 levels by 30 .+-. 2% (P < 0.01) and serum T3 levels by 35 .+-. 4% (P < 0.001). However free T4 and T3 fractions increased markedly within the first 140 min by 162 .+-. 20% (P < 0.001) and by 55 .+-. 4% (P < 0.001) resulting in a 88 .+-. 20% increase in the free T4 concentration (P < 0.001) but no increase in the free T3 concentration. Serum TSH concentration fell in the 5 h after the hrIL-1 injection by 77 .+-. 3% (P < 0.001). A similar decrease was observed with 0.125 .mu.g hrIL-1. Five hours of starvation did not change serum TSH levels, suggesting that the effect of hrIL-1 on TSH was not due to decreased food intake. In order to test whether the decrease in serum TSH was due to an intrapituitary increase in T3, hrIL-1 was injected in hypothyroid rats: the fall of serum TSH was not prevented and it fell in 5 h from 14.05 .+-. 0.56 to 9.66 .+-. 0.98 ng/ml (31%, P < 0.01, n = 14). These results suggest that hrIL-1 acts independently of thyroid hormones. Peripheral metabolism of T4 was studied by implanting [125]T4 secreting minipumps during days. There was no differences in T4 plasma clearance rate between control and treated animals. The fall of serum T4 was therefore explained by decreased secretion and not by increased catabolism since either link cleavage of T4 and changes in hepatic deiodinase could not be detected. We therefore suggest that hrIL-1 inhibits thyroid function mainly at the hypothalamic-hypophyseal level.