Type 1 and type 2 iodothyronine deiodinases in the thyroid gland of patients with 3,5,3′-triiodothyronine-predominant Graves' disease

2011 ◽  
Vol 2011 ◽  
pp. 118-120
Author(s):  
M. Schott
Keyword(s):  
Thyroid Gland ◽  
Graves Disease ◽  
Iodothyronine Deiodinases

scholarly journals Type 1 and type 2 iodothyronine deiodinases in the thyroid gland of patients with 3,5,3′-triiodothyronine-predominant Graves' disease

2011 ◽  
Vol 164 (1) ◽  
pp. 95-100 ◽  
Author(s):  
Mitsuru Ito ◽  
Nagaoki Toyoda ◽  
Emiko Nomura ◽  
Yuuki Takamura ◽  
Nobuyuki Amino ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Mrna Level ◽  
Antithyroid Drug ◽  
High Serum ◽  
Graves Disease ◽  
Iodothyronine Deiodinase ◽  
Iodothyronine Deiodinases ◽  
Antithyroid Drug Therapy

Objective3,5,3′-triiodothyronine-predominant Graves' disease (T3-P-GD) is characterized by a persistently high serum T3 level and normal or even lower serum thyroxine (T4) level during antithyroid drug therapy. The source of this high serum T3 level has not been clarified. Our objective was to evaluate the contribution of type 1 and type 2 iodothyronine deiodinase (D1 (or DIO1) and D2 (or DIO2) respectively) in the thyroid gland to the high serum T3 level in T3-P-GD.MethodsWe measured the activity and mRNA level of both D1 and D2 in the thyroid tissues of patients with T3-P-GD (n=13) and common-type GD (CT-GD) (n=18) who had been treated with methimazole up until thyroidectomy.ResultsThyroidal D1 activity in patients with T3-P-GD (492.7±201.3 pmol/mg prot per h) was significantly higher (P<0.05) than that in patients with CT-GD (320.7±151.9 pmol/mg prot per h). On the other hand, thyroidal D2 activity in patients with T3-P-GD (823.9±596.4 fmol/mg prot per h) was markedly higher (P<0.005) than that in patients with CT-GD (194.8±131.6 fmol/mg prot per h). There was a significant correlation between the thyroidal D1 activity in patients with T3-P-GD and CT-GD and the serum FT3-to-FT4 ratio (r=0.370, P<0.05). Moreover, there was a strong correlation between the thyroidal D2 activity in those patients and the serum FT3-to-FT4 ratio (r=0.676, P<0.001).ConclusionsOur results suggest that the increment of thyroidal deiodinase activity, namely D1 and especially D2 activities, may be responsible for the higher serum FT3-to-FT4 ratio in T3-P-GD.

Type 1 and type 2 iodothyronine deiodinases in the thyroid gland of patients with huge goitrous Hashimoto’s thyroiditis

Endocrine ◽  
2019 ◽  
Vol 64 (3) ◽  
pp. 584-590 ◽  
Author(s):  
Azusa Harada ◽  
Emiko Nomura ◽  
Kumiko Nishimura ◽  
Mitsuru Ito ◽  
Hiroshi Yoshida ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Iodothyronine Deiodinases

scholarly journals Synthesis and Metabolism of Thyroid Hormones Is Preferentially Maintained in Selenium-Deficient Transgenic Mice

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1306-1313 ◽  
Author(s):  
Lutz Schomburg ◽  
Cornelia Riese ◽  
Marten Michaelis ◽  
Emine Griebert ◽  
Marc O. Klein ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Knockout Mice ◽  
Serum Levels ◽  
Mrna Levels ◽  
Normal Range ◽  
Growth Defects ◽  
Low Levels

The thyroid gland is rich in selenium (Se) and expresses a variety of selenoproteins that are involved in antioxidative defense and metabolism of thyroid hormones (TH). Se deficiency impairs regular synthesis of selenoproteins and adequate TH metabolism. We recently generated mice that lack the plasma Se carrier, selenoprotein P (SePP). SePP-knockout mice display decreased serum Se levels and manifest growth defects and neurological abnormalities partly reminiscent of thyroid gland dysfunction or profound hypothyroidism. Thus, we probed the TH axis in developing and adult SePP-knockout mice. Surprisingly, expression of Se-dependent 5′-deiodinase type 1 was only slightly altered in liver, kidney, or thyroid at postnatal d 60, and 5′-deiodinase type 2 activity in brain was normal in SePP-knockout mice. Thyroid gland morphology, thyroid glutathione peroxidase activity, thyroid Se concentration, and serum levels of TSH, T4, or T3 were within normal range. Pituitary TSHβ transcripts and hepatic 5′-deiodinase type 1 mRNA levels were unchanged, indicating regular T3 bioactivity in thyrotropes and hepatocytes. Cerebellar granule cell migration as a sensitive indicator of local T3 action during development was undisturbed. Collectively, these findings demonstrate that low levels of serum Se or SePP in the absence of other challenges do not necessarily interfere with regular functioning of the TH axis. 5′-deiodinase isozymes are preferentially supplied, and Se-dependent enzymes in the thyroid are even less-dependent on serum levels of Se or SePP than in brain. This indicates a top priority of the thyroid gland and its selenoenzymes with respect to the hierarchical Se supply within the organism.

Endocrine autoimmunity

2011 ◽  
pp. 34-44 ◽  
Author(s):  
Matthew J. Simmonds ◽  
Stephen C. L. Gough
Keyword(s):  
Immune Response ◽  
Type 1 Diabetes ◽  
Immune System ◽  
Endocrine System ◽  
Graves Disease ◽  
Self Tolerance ◽  
Autoimmune Attack ◽  
Endocrine Organs

Dysfunction within the endocrine system can lead to a variety of diseases with autoimmune attack against individual components being some of the most common. Endocrine autoimmunity encompasses a spectrum of disorders including, e.g., common disorders such as type 1 diabetes, Graves’ disease, Hashimoto’s thyroiditis, and rarer disorders including Addison’s disease and the autoimmune polyendocrine syndromes type 1 (APS 1) and type 2 (APS 2) (see Table 1.6.1). Autoimmune attack within each of these diseases although aimed at different endocrine organs is caused by a breakdown in the immune system’s ability to distinguish between self and nonself antigens, leading to an immune response targeted at self tissues. Investigating the mechanisms behind this breakdown is vital to understand what has gone wrong and to determine the pathways against which therapeutics can be targeted. Before discussing how self-tolerance fails, we first have to understand how the immune system achieves self-tolerance.

scholarly journals Sources of Circulating 3,5,3′-Triiodothyronine in Hyperthyroidism Estimated after Blocking of Type 1 and Type 2 Iodothyronine Deiodinases

2007 ◽  
Vol 92 (6) ◽  
pp. 2149-2156 ◽  
Author(s):  
Peter Laurberg ◽  
Henrik Vestergaard ◽  
Soren Nielsen ◽  
Stig E. Christensen ◽  
Torben Seefeldt ◽  
...  
Keyword(s):  
Iodothyronine Deiodinases

scholarly journals Free thyroid hormons ration in patients with amiodaron-induced thyrotoxicosis type 1 and type 2

2018 ◽  
Vol 5 (3) ◽  
pp. 28-35
Author(s):  
E. O. Ulupova ◽  
G. A. Bogdanova ◽  
T. L. Karonova ◽  
E. N. Grineva
Keyword(s):  
Doppler Sonography ◽  
Graves Disease ◽  
Additional Test ◽  
Diagnostic Challenge ◽  
Color Flow ◽  
Serum T4 ◽  
Color Flow Doppler Sonography ◽  
Effect Of Treatment

Differentiation between amiodarone-induced thyrotoxicosis type 1 (AmIT1) and type 2 (AmIT2) is a diagnostic challenge. The current diagnostic tests are often unable to differentiate these two types of thyrotoxic syndrome. Several studies had shown that the serum T4 level and T3/T4 ratio are significantly different in patients with destructive thyroiditis, and those with Graves` disease. These studies showed that the serum T4 concentration is significantly higher, and the T3/T4 ratio is significantly lower in patients with destructive forms of thyroiditis compared to their values  in Graves’ disease. Since AmIT1 is known to develop in patients with latent Graves` disease, and AmIT2 is a destructive thyroiditis, the purpose of our study was to evaluate the serum FТ4 level and FT4/FT3 ratio in AmIT1 and AmIT2 as an additional diagnostic test for differentiating these types of thyrotoxicosis. 45 patients with thyrotoxicosis (33 with AmIT1 and 12 AmIT2) were included in the study. The diagnosis of thyrotoxicosis type (AmIT1 or AmIT2) was established on the basis of clinical data, color flow Doppler sonography (CFDS), the presence of TSH receptor autoantibody in patients with AmIT1, as well as the effect of treatment. There was no difference in FT3 levels in patients with AmIT1 and AmIT2, while the FT4 values were significantly higher in patients with AmIT2 (36,2±19,1 mmol/L) than in those with AmIT1 (17,8±3,7 mmol/L, p= 0,002). Also, a difference in the FT4/FT3 ratio was found between AmIT1 (2,7±0,8) and AmIT2 (6,1±5,7, p=0,048). Moreover, 75% of patients with AmIT1 had FT4/FT3ratio < 3,10, while 75% of patients with AmIT2 had FT4/FT3 ratio > 3,65. The FT4/FT3 ratio can be used as an additional test in the differential diagnosis AmIT1 and AmIT2.

scholarly journals Thyroid over-expression of type 1 and type 2 deiodinase may account for the syndrome of low thyroxine and increasing triiodothyronine during propylthiouracil treatment

2003 ◽  
pp. 443-447 ◽  
Author(s):  
AP Weetman ◽  
CA Shepherdley ◽  
P Mansell ◽  
CS Ubhi ◽  
TJ Visser
Keyword(s):  
Thyroid Tissue ◽  
Graves Disease ◽  
Similar Response ◽  
Over Expression ◽  
Thyroid Stimulating Antibodies ◽  
Hormone Profile ◽  
Rapid Fall ◽  
Very High

Although propylthiouracil inhibits type 1 deiodinase, leading to a more rapid fall in triiodothyronine (T(3)) than thyroxine (T(4)) levels in patients treated for hyperthyroidism, we report a patient with Graves' disease whose free T(3) paradoxically rose during such treatment, despite low free T(4) levels and increasing doses of propylthiouracil. A similar response has previously been associated with high levels of thyroid stimulating antibodies, but it has been unclear why there should be a dichotomy in the circulating thyroid hormone profile. Thyroid tIssue from our patient contained very high levels of type 1 and, especially, type 2 deiodinase, in contrast to other patients treated with Graves' disease, which were most likely secondary to high levels of thyroid stimulating antibodies. This unusual response to propylthiouracil is important to recognise therapeutically, and represents a further situation in which abnormal expression of deiodinase enzymes has clinical significance.

scholarly journals Comparative kinetic characterization of rat thyroid iodotyrosine dehalogenase and iodothyronine deiodinase type 1

2004 ◽  
Vol 181 (3) ◽  
pp. 385-392 ◽  
Author(s):  
JC Solis-S ◽  
P Villalobos ◽  
A Orozco ◽  
C Valverde-R
Keyword(s):  
Thyroid Gland ◽  
Distinct Group ◽  
Kinetic Properties ◽  
Iodothyronine Deiodinase ◽  
Iodothyronine Deiodinases ◽  
Iodine Metabolism ◽  
Rat Thyroid ◽  
Rat Thyroid Gland

The initial characterization of a thyroid iodotyrosine dehalogenase (tDh), which deiodinates mono-iodotyrosine and di-iodotyrosine, was made almost 50 years ago, but little is known about its catalytic and kinetic properties. A distinct group of dehalogenases, the so-called iodothyronine deiodinases (IDs), that specifically remove iodine atoms from iodothyronines were subsequently discovered and have been extensively characterized. Iodothyronine deiodinase type 1 (ID1) is highly expressed in the rat thyroid gland, but the co-expression in this tissue of the two different dehalogenating enzymes has not yet been clearly defined. This work compares and contrasts the kinetic properties of tDh and ID1 in the rat thyroid gland. Differential affinities for substrates, cofactors and inhibitors distinguish the two activities, and a reaction mechanism for tDh is proposed. The results reported here support the view that the rat thyroid gland has a distinctive set of dehalogenases specialized in iodine metabolism.

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