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Deiodination and Peripheral Metabolism of Thyroid Hormone

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The Thyroid and Its Diseases

Abstract

Canonical thyroid hormone (TH) signaling results from the interaction of T3 with nuclear receptors and stimulation or repression target genes. Ligand (T3) availability is under tight control of several intracellular checkpoints, which enable target cells to modify their own T3 fingerprint. A crucial step of intracellular T3 metabolism is catalyzed by the deiodinases. These enzymes can, within the single cell, enhance (D1 and D2) or reduce (D3) T3 concentrations. Thyroid hormone transport within the target cells is also a limiting step of thyroid hormone action. Various specific transporters have been isolated for the entrance and the clearance of the iodothyronines and constitute a complex system of active transport of THs inside and outside the cells. Concerted modulation of the different TH regulating factors is responsible for a spatiotemporal precise adaptation of the hormonal signal to the different cell-specific requirements.

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Dentice, M., Salvatore, D. (2019). Deiodination and Peripheral Metabolism of Thyroid Hormone. In: Luster, M., Duntas, L., Wartofsky, L. (eds) The Thyroid and Its Diseases. Springer, Cham. https://doi.org/10.1007/978-3-319-72102-6_5

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