Type 2 iodothyronine deiodinase is highly expressed in human thyroid.

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

doi:10.1172/jci118880

Cited by 196Thyroid Disorders and TreatmentsThyroid Cancer Diagnosis and TreatmentSelenium in Biological Systems

Type 2 iodothyronine deiodinase is highly expressed in human thyroid.

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Salvatore, D, Tu, H, Harney, J W, Larsen, P R·1996·Journal of Clinical Investigation

DOI 10.1172/jci118880PMC PMC507511

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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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D2 activity in humans has been detected in various tissues, predominantly in the central nervous system, pituitary gland, thyroid, heart, brown adipose tissue, and skeletal muscle (15-17).
“D2 activity in humans has been detected in various tissues, predominantly in the central nervous system, pituitary gland, thyroid, heart, brown adipose tissue, and skeletal muscle (1517).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [16]
The Introduction (page unavailable) reports D2 activity in human brown adipose tissue, pituitary tumors, and skeletal muscle; the Discussion reports activity in human thyroid. For human cerebral cortex and cardiac muscle, the Introduction reports D2 mRNA rather than enzyme activity. Its pituitary activity finding concerns tumors, not the pituitary gland generally. (LLM, conf=0.88)
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TSHR-mediated upregulation of DIO2 contributes significantly to the relative increase in intrathyroidal T4-to-T3 conversion and thus T3 production and higher circulating T3/T4 ratio in patients with Graves' disease and toxic adenomas.
“TSHR-mediated upregulation of DIO2 contributes significantly to the relative increase in intrathyroidal T4-to-T3 conversion and thus T3 production and higher circulating T3/T4 ratio in patients with Graves’ disease and toxic adenomas (182, 183).”
From Intrathyroidal feedforward and feedback network regulating thyroid hormone synthesis and secretion (2022) · cites this paper as [182]
The Abstract reports greater D2-mediated T4-to-T3 conversion in stimulated thyroids and concludes that it may contribute significantly to increased thyroidal T3 production in Graves’ disease and toxic adenomas. The Discussion proposes TSH-related signaling as an explanation for high D2 expression but says other factors remain unidentified. The paper does not establish TSHR-mediated upregulation as the cause or directly show that D2 raises the circulating T3/T4 ratio; section labels are available, but passage page numbers are not. (LLM, conf=0.87)
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Short title: Deiodinase in T3-predominant Graves ’ disease
Ito, M., Toyoda, N., Nomura, E., Takamura, Y., Amino, N., Iwasaka, T., Takamatsu, J., Miyauchi, A., Nishikawa, M., Deiodinase, K. W., et al. (2016)

Authors: Salvatore, D., Tu, H., Harney, J. W., & Larsen, P. R.
Affiliations: Brigham and Women's Hospital (US)
Corresponding author: Larsen, P R
ORCID: Salvatore, D
Tu, H
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1996-08-15
Volume: 98
Issue: 4
Pages: 962-968
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci118880
PMC: PMC507511
OpenAlex: W2011717087
Cited by: 196
References: 42
Citations by year: 2026: 1 · 2025: 3 · 2024: 1 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 6 · 2019: 3 · 2018: 5 · 2017: 3 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 3 · 2012: 6
FWCI: 7.79
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (DK36256, R01DK036256, T32DK007529, DK-07529)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
Keywords: type 2 deiodinase, type 1 iodothyronine deiodinase, thyroid gland, triiodothyronine, T4 to T3 conversion, Graves' disease, follicular adenoma, multinodular goiter, TSH stimulation, propylthiouracil, iodine deficiency, thyroid hormone metabolism
MeSH terms: Enzyme Inhibitors, Humans, Iodide Peroxidase, Isoenzymes, Kinetics, Microsomes, Placenta, Propylthiouracil, RNA, Messenger, Thyroid Gland, Thyroxine, Triiodothyronine, Gene Expression

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Type 2 iodothyronine deiodinase is highly expressed in human thyroid.

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