Ikeda T, Ito Y, Murakami I, Mokuda O, Tominaga M, Mashiba H
Acta Endocrinol (Copenh). 1986 May;112(1):89-92. doi: 10.1530/acta.0.1120089.
To evaluate the effect of hepatocellular damage on thyroid hormone metabolism, the conversion of T4 to T3 in the perfused liver of rats with carbontetrachloride (CCl4)-induced liver injury was investigated. The liver was perfused non-recyclically with a synthetic medium containing 10 micrograms/dl T4 for 30 min, and the T3 production and the conversion of T4 to T3 were examined. The serum T3 level was significantly (P less than 0.05) lower in liver-injury rats (72 +/- 9 ng/dl) compared with controls (88 +/- 10 ng/dl). The uptake of T4 (4.15 +/- 0.85 micrograms/g/30 min), net T3 production (180 +/- 48 ng/g/30 min), and conversion rate of T4 to T3 (4.4 +/- 0.9%) in the perfused liver of liver-injury rats were similar to the values (3.78 +/- 0.66 micrograms/g/30 min, 191 +/- 31 ng/g/30 min, and 5.0 +/- 1.0%) in control rats, whereas the release of T3 (12.7 +/- 3.2 ng/g/30 min) in the effluent in injured livers was significantly (P less than 0.05) lower than that (16.9 +/- 3.0 ng/g/30 min) in control livers. We concluded that in CCl4-induced liver-injury rats, the low serum T3 level may partly be due to the decreased release of T3 from liver cells after conversion of T4 to T3 rather than to a decreased conversion of T4 to T3.
