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. 2022 Nov 22;44(3):393–416. doi: 10.1210/endrev/bnac030

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© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 6. — (A) The rendering of 2D inkjet printing. The ratio of T3 to T4 can be modified by printer. (B) The counter regulatory mechanism of T3S. T3S is a biologically inactive derivate of T3 and serves as its reserve pool. T3S is mainly converted to inactive T2S by D1. D1 activity is directly regulated by T3, namely, high T3 levels accelerate T3S deiodination, leaving less T3S available for desulfation. Consequently, less T3 in produced. (C) The release and adherence of poly-zinc-T3 in vivo. PZLs leak out from capsules on entry into intestine and adhere to epithelium mucosa through ionic interaction. PZL gradually degrades and T3 is thus released and absorbed. Abbreviations: T2S, 3,3′-diiodothyronine sulfate; T3S, triiodothyronine sulfate; S, sulfate. The figure was partly generated using illustrative elements from Servier Medical Art, provided by Servier, licensed under a Creative Commons Attribution 3.0 unported license.