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Effect of Dexamethasone on Triiodothyronine Production in the Perfused Rat Liver and Kidney^*

Department of Medicine, Endocrine Section, University of Pennsylvania School of Medicine Philadelphia, Pennsylvania 19104

Address requests for reprints to: Dr. Anthony S. Jennings, Endocrine Section, University of Pennsylvania School of Medicine, 527 Johnson Pavilion G2, 36th and Hamilton Walk, Philadelphia, Pennsylvania 19104.

Abstract

Dexamethasone administration to rats decreases T₄-5'-deiodinase activity in liver homogenates and slices and in isolated rat renal tubules. To determine if this decreased T₄-5'-deiodinase activity results in decreased T₃ production, rat livers and kidneys of control and dexamethasone-treated rats were perfused with medium containing free T₄ concentrations approximating euthyroid rat serum, and net T₃ production was measured by RIA. Dexamethasone administration decreased body weight by 14% but did not affect liver weight, kidney weight, or serum concentrations of T₄ or T₃. When livers were perfused with T₄ concentrations of 10 µg/dl (free T₄ = 6.5 ng/ dl), hepatic T₃ production, T₄ uptake, and the conversion of T₄ to T₃ were similar in dexamethasone-treated rats and salinetreated controls. However, when livers were perfused at a T₄ concentration of 125 µg/dl (free T₄ = 81 ng/dl), dexamethasonetreated livers produced significantly less T₃ than controls because of decreased conversion of T₄ to T₃. Hepatic deiodination of T₃ and excretion of T₃ into bile were not affected by dexamethasone. Renal T₃ production, T₄ uptake, and conversion of T₄ to T₃ was likewise unaffected by dexamethasone treatment when kidneys were perfused at near-normal free T₄ concentrations. These studies indicate that dexamethasone treatment does not alter T₃ production in the perfused liver and kidney and underscore the importance of using free T₄ concentrations approximating physiologic levels when studying regulation of T₃ production in individual organs. (Endocrinology 114: 31, 1984)

Footnotes

^* This work was supported by NIH Grants 5-F32-AM-0851-02, 2-P30-AM-19525-05, and 5-R23-AM-30532-02.

Received May 27, 1983.

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