Human Recombinant Interleukin-1β Decreases Plasma Thyroid Hormone and Thyroid Stimulating Hormone Levels in Rats*

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Abstract
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.