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Research Article Free access | 10.1172/JCI118880

Type 2 iodothyronine deiodinase is highly expressed in human thyroid.

D Salvatore, H Tu, J W Harney, and P R Larsen

Thyroid Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Salvatore, D. in: JCI | PubMed | Google Scholar

Thyroid Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Tu, H. in: JCI | PubMed | Google Scholar

Thyroid Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Harney, J. in: JCI | PubMed | Google Scholar

Thyroid Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Larsen, P. in: JCI | PubMed | Google Scholar

Published August 15, 1996 - More info

Published in Volume 98, Issue 4 on August 15, 1996
J Clin Invest. 1996;98(4):962–968. https://doi.org/10.1172/JCI118880.
© 1996 The American Society for Clinical Investigation
Published August 15, 1996 - Version history
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Abstract

Type 2 iodothyronine deiodinase (D2) is a recently cloned selenodeiodinase thought to provide intracellular 3,5,3' triiodothyronine (T3) to a restricted group of tissues. We report here the presence of D2 mRNA in human thyroid at levels 50-150-fold higher than in placenta. Surprisingly, while type 1 deiodinase (D1) is known to be present in human thyroid, D2 has not been evaluated previously. D2 mRNA was especially high in thyroids from Graves' patients and in follicular adenomas. Stimulated thyroids had higher D2 to D1 mRNA ratios than normal or multinodular glands suggesting differential regulation of D1 and D2 expression. Microsomes from normal, Graves', and TSH-stimulated thyroids contained low Km D2 activity resistant to propylthiouracil (1 mM) or to inactivation by N-bromoacetyl T3, agents which block or inactivate D1. At 2 nM thyroxine (T4), 100 times the physiological-free T4 levels, 60-80% of T4 to T3 conversion in stimulated, but only 27% of that in normal thyroids, is catalyzed by D2. We conclude that intrathyroidal T4 to T3 conversion by D2 may contribute significantly to the relative increase in thyroidal T3 production in patients with Graves' disease, toxic adenomas, and, perhaps, iodine deficiency.

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