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The pleiotropic inhibitory effects of excess iodine on the thyroid gland are well known. All the steps leading to thyroid hormone secretion are affected: iodide uptake, iodide organification and the secretory process itself (see Ref. 1 for a review). From A teleological viewpoint, the rationale of these inhibitory effects is straightforward. As an adaptation to the scarcity of iodine in the environment and the variability of its dietary intake, the thyroid cells are equipped with efficient mechanisms of uptake and storage, designed to optimize its use. However, this efficiency would lead to a risk of thyrotoxicosis in case of a sudden exposure to an abundant supply of iodine if there was no homeostatic regulation. Facing the multiplicity of the inhibitory actions of excess iodine, there is a need to go beyond their mere description and to identify a limited number of biochemical mechanisms. One mechanism is certainly the uncoupling between
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