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PubMed1984

Acute ingestions of thyroid hormones.

Although thyroid medications are commonly prescribed, there are only nine case reports describing the consequences of acute excessive ingestion of thyroid hormones. Two additional cases are presented and the prior nine cases are reviewed. The potential for toxicity is discussed in relationship to the cellular mechanisms of action of thyroid hormones. Although the potential for toxicity is low, the following therapy is recommended to decrease further the toxic potential: (1) lavage and activated charcoal to decrease absorption, (2) cholestyramine to decrease enterohepatic circulation (3) prednisone and/or propylthiouracil to decrease conversion of thyroxine to triiodothyronine, and (4) propranolol to block metabolic effects. If symptoms of toxicity develop, then attempts to remove thyroid hormones should be undertaken using exchange transfusion.

Acute Disease↗

PubMed1997

Mutation in the thyroid hormone receptor beta gene (A317T) in a Thai subject with resistance to thyroid hormone.

Analysis of the thyroid hormone receptor beta (TRbeta) gene of a Thai female with the syndrome of resistance to thyroid hormone (RTH) revealed a missense mutation at codon 317, changing the guanine in nucleotide 1234 to an adenine that results in the replacement of the normal alanine (GCT) with a threonine (ACT). The proposita was heterozygous, and this mutation was not present in her parents and her sister, compatible with a neomutation. This is the first report of TRbeta gene mutation causing RTH in an individual of Thai origin.

Amino Acid Substitution↗

PubMed1995

Effect of thyrotropin-releasing hormone on serum thyroid hormones: a study in the patients with untreated and treated Graves' disease and subacute thyroiditis.

In order to investigate the extrapituitary action of TRH on the thyroid, serum T3, T4, and TSH levels after im administration of TRH were analyzed in 63 patients with untreated hyperthyroid Graves' disease, in 60 euthyroid patients with treated Graves' disease, in 8 patients with subacute thyroiditis, and in 140 healthy subjects. TRH administration in the healthy subjects resulted in a significant increase in serum T3 and T4 levels after 2 h. However, in the patients with untreated hyperthyroid Graves' disease, a significant decrease in serum T3 and T4 levels with undetectable TSH was found 2 h after TRH administration. In the patients with subacute thyroiditis, serum T3 levels also significantly decreased after TRH administration. When a decrease in serum T3 and T4 levels after TRH administration in the patients with hyperthyroid Graves' disease was analyzed in terms of thyroid microsomal antibody and thyroglobulin antibody, a decrease in serum T3 and T4 levels was largest in patients with thyroid microsomal antibody and thyroglobulin antibody. In contrast, an increase in serum T3 and T4 levels in response to TRH in the euthyroid patients with Graves' disease was largest in patients without thyroid autoantibodies. It is concluded that TRH acts directly on the thyroid to suppress the thyroid hormone secreting activity in the absence of circulating TSH and that thyroid autoantibodies affect thyroidal response after TRH administration.

Adolescent↗

PubMed1992

Rapid localization of mutations in the thyroid hormone receptor-beta gene by denaturing gradient gel electrophoresis in 18 families with thyroid hormone resistance.

Generalized resistance to thyroid hormone (GRTH) is an inherited syndrome of reduced tissue responsiveness to thyroid hormone. Point mutations in the human thyroid hormone receptor-beta (hTR beta) gene of these patients, causing single amino acid substitutions, appear be different in unrelated individuals affected by the same syndrome. To localize mutations in the hTR beta gene, GC-clamped DNA fragments from affected individuals belonging to 21 families with GRTH were generated by the polymerase chain reaction and analyzed by denaturing gradient gel electrophoresis (DGGE). Putative mutations in the hTR beta gene of 18 unrelated individuals with GRTH were identified, and their nature has been confirmed in 9 by sequencing. All were in the hormone-binding domain of the receptor, and 13 of 18 mutations were in its center (exon 7). In 3 families we were unable to identify mutations in hTR beta, suggesting the existence of mutations at other loci, possibly the hTR alpha gene or other proteins involved in the thyroid hormone-dependent transactivation system. Sequencing of DNA fragments negative for the presence of putative mutations by DEEG confirmed the absence of sequence differences. DGGE of amplified DNA fragments can rapidly and reliably localize the sites of mutations in the hTR beta gene of patients with GRTH. The procedure enabled mapping the regions in the hTR beta harboring mutations associated with GRTH.

Base Sequence↗

PubMed1997

Deoxyribonucleic acid binding and transcriptional silencing by a truncated c-erbA beta 1 thyroid hormone receptor identified in a severely retarded patient with resistance to thyroid hormone.

We describe the analysis of a thyroid hormone receptor (TR) beta causing resistance to thyroid hormone, the patient exhibiting hypothyroid symptoms (severe mental retardation, hypoactivity, obesity) and hyperthyroid symptoms (tachycardia, low serum cholesterol) and, additionally, relative early puberty, advanced bone age, and short stature. The patient was heterozygous, with a point mutation producing a premature stop-codon in TR beta-gene exon 10, resulting in a 28-amino acid carboxy-terminal deletion in the cognate TR beta (TR beta-EZ). T3 binding was abolished. Homodimer binding of TR beta-EZ to DR4- and F2-T3 response elements (TREs) was weaker, and to a palindromic TRE (PAL) was stronger than that of wild-type TR beta (TR beta-WT) in the absence of T3. T3 dissociated TR beta-WT, but not TR beta-EZ homodimer, from DR4, F2, and Pal. Heterodimerization of TR beta-EZ with retinoid x receptor beta was seen. TR beta-EZ repressed basal thymidine kinase-promotor activity, coupled to DR4, F2, or PAL. Silencing of basal gene transcription via PAL was weaker, and via DR4 and F2 was more pronounced, compared with TR beta-WT. TR beta-EZ had a strong dominant negative effect on TR beta-WT, attenuated in a TRE- and cell-specific manner by high T3 concentrations. Finally, the degree of TR beta-EZ homodimer-binding affinity to DNA did not correlate with the degree of transcriptional dominant negative activity.

Adolescent↗

PubMed1997

Transcriptional induction of RC3/neurogranin by thyroid hormone: differential neuronal sensitivity is not correlated with thyroid hormone receptor distribution in the brain.

RC3/neurogranin is a calmodulin-binding protein kinase C substrate, located in dendritic spines of forebrain neurons. It has been implicated in post-synaptic signal transduction events involving Ca2+ and calmodulin leading to many forms of synaptic plasticity. RC3 gene expression is under developmental and physiological regulation. The main physiological regulator appears to be thyroid gland activity. Hypothyroidism decreased RC3 mRNA concentration in the brain of post-natal day 22 rats. The affected areas included layer 6 of cerebral cortex, layers 2-3 of retrosplenial cortex, dentate gyrus and the caudate whereas others were not affected by hypothyroidism, such as upper layers of cerebral cortex, the pyramidal layer of the hippocampus and the amygdala. A single administration of triiodothyronine (T3) induced a significant transcriptional increase of RC3 mRNA in hypothyroid rats, 24 h after administration. Differential sensitivity to thyroid hormone was not related to differential expression of T3 receptor isoforms or the T3 receptor inhibitory variant alpha2. Therefore, it is likely that cell sensitivity to thyroid hormone in the brain depends on T3 receptor-associated factors.

Animals↗

PubMed1993

Prevalence of subclinical hyperthyroidism and relationship between thyroid hormonal status and thyroid ultrasonographic parameters in patients with non-toxic nodular goitre.

OBJECTIVE: Basal plasma T4, T3 and TSH concentrations are usually normal in patients presenting with non-toxic nodular goitre. Using the evaluation of TSH response to TRH in a large series of such patients living in an area with normal iodine intake, we evaluated the prevalence of subclinical hyperthyroidism and the relationship between thyroid hormonal status and ultrasonographic parameters. PATIENTS: A prospective study of 242 consecutive patients (group I), referred with non-autoimmune nodular goitre, normal plasma free T4, total T3 and TSH levels, without (subgroup IA, 222 patients) or with (subgroup IB, 20 patients) clear-cut autonomous area(s) on scintigraphy. These patients were compared to 135 controls (group II). MEASUREMENTS: Plasma free T4 (FT4), total T3 (T3T) and TSH measurements. Evaluation of TSH response to TRH (delta level of increased TSH = peak TSH level during TRH test-basal TSH level), thyroid scintigraphy and morphological characteristics (number and total volume of nodule(s) and volume of extranodular tissue) determined by ultrasonography. RESULTS: In subgroup IA, (1) the mean (+/- SEM) basal TSH level (0.94 +/- 0.04 mU/I) and the mean value of increased TSH after TRH (4.92 +/- 0.34 mU/I) were lower (P < 0.001) than in group II (1.28 +/- 0.05 mU/I and 7.24 +/- 0.25 mU/I, respectively). The prevalence of SH (delta level of increased TSH below the mean -3 SD in controls) was 17.2%; (2) the mean FT4 level and the mean T3T value were not different (P > 0.05) from those of group II. In subgroup IB, (1) the mean basal TSH level (0.57 +/- 0.11 mU/I) and the mean increment of TSH after TRH (2.81 +/- 0.62 mU/I) were lower (P < 0.001) than in subgroup IA. The prevalence of subclinical hyperthyroidism was 75.0%; (2) the mean FT4 level (17.2 +/- 0.9 pmol/I) was not different from that in group II. However, the mean T3T value (1.99 +/- 0.01 nmol/I) was higher (P < 0.001) than in group II (1.65 +/- 0.05). In group I, subgroup IA and IB, there were significant (P < 0.05, at least) correlations between the numbers of nodules and both basal TSH levels and delta values of increased TSH or FT4 levels or T3T values. No correlations were found between other ultrasonographic data and plasma thyroid parameters. CONCLUSIONS: This study demonstrates a high prevalence of subclinical hyperthyroidism in patients presenting with non-toxic nodular goitres and suggests that the number of nodules, but not their total volume, is an important factor in the development of this condition.

Adolescent↗

PubMed2001

Physiological and molecular basis of thyroid hormone action.

Thyroid hormones (THs) play critical roles in the differentiation, growth, metabolism, and physiological function of virtually all tissues. TH binds to receptors that are ligand-regulatable transcription factors belonging to the nuclear hormone receptor superfamily. Tremendous progress has been made recently in our understanding of the molecular mechanisms that underlie TH action. In this review, we present the major advances in our knowledge of the molecular mechanisms of TH action and their implications for TH action in specific tissues, resistance to thyroid hormone syndrome, and genetically engineered mouse models.

Amino Acid Sequence↗

PubMed2005

Evaluation of gene expression endpoints in the context of a Xenopus laevis metamorphosis-based bioassay to detect thyroid hormone disruptors.

Thyroid hormones (TH) are important in growth, development and the maintenance of proper cellular metabolism in vertebrates. Amphibian metamorphosis is completely dependent on TH and forms the basis of a screen for thyroid axis disrupting chemicals that currently relies on external morphological endpoints and changes in thyroid gland histology. The requirement for TH-dependent gene expression makes it possible to augment this screen through the addition of molecular endpoints. In order to do this, gene selection, choice of sampling time, tissue sensitivity, and their relationship to morphological change must all be considered. We exposed stage 54 Xenopus laevis tadpoles to a concentration series of the THs, thyroxine (T4) and 3,5,3'-triiodothyronine (T3), and three known TH antagonists, methimazole, propylthiouracil (PTU), and perchlorate. The agonists significantly accelerated metamorphosis as defined by developmental stage attained after 14 days. In contrast, the TH antagonists significantly delayed metamorphosis at 14 days and caused an increase in thyroid gland size at day 8. We assessed the changes in steady-state mRNA levels of thyroid hormone receptor alpha- and beta-isoforms and the basic transcription element binding (BTEB) protein by quantitative real-time polymerase chain reaction. Three tissues (brain, tail and hindlimb) were analyzed at 24, 48 and 96 h and we found that TH receptor, TRbeta, and BTEB were the most sensitive gene transcripts for the TH agonists, whereas only TRalpha displayed significant changes upon antagonist exposure. We detected differences in tissue-specific responses between the two agonists. We matched the concentrations of T3 and T4 that elicited similar biological responses at 14 days and compared the induction of gene expression. At 96 h, the TRbeta and BTEB expression response to T3 and T4 was similar in the tail. In contrast, T3 elicited no concentration-dependent changes in TRbeta and BTEB expression in the brain, whereas T4 elevated their expression. The tail showed the highest correlation between TH concentration and morphological outcome whereas the brain was the most sensitive to antagonist treatment. Only methimazole and perchlorate showed significant changes in TRalpha gene expression in the brain whereas PTU did not suggesting differences in cellular mechanisms of action. The greatest effect on gene expression occurred within 48 h with many of the hormone-dependent changes disappearing by 96 h. This study accentuates the need to examine multiple tissues and provides critical information required for optimization of exposure regimens and endpoint assessments that focus on the detection of disruption in TH-regulatory systems.

Animals↗

PubMed2004

[Thyroid hormone levels and thyroid dysfunction of French adults participating in the SU.VI.MAX study].

Abnormal thyroid function has important public health consequences. However, the various degrees of thyroid dysfunction remain unsettled. The SU.VI.MAX cohort provided a unique opportunity to conduct a cross-sectional study of abnormal thyroid function in a large representative population of 11256 men and women representing the geographic distribution of the French continental adult population. Thyroid status was measured, in fasting blood samples, at baseline in 1994-1995. Serum thyrotropin (TSH) levels (abnormal < 0.4 mU/l or > or =4.0 mU/l) and free thyroxine (fT4) were both performed in duplicate on the same sample. Subjects with previous or present thyroid diseases or who were taking thyroid hormones or antithyroid drugs (n=920) were excluded (8.1%). Thus, the final study group consisted of 10346 subjects, 4121 men aged 45-60 years (mean +/-SD) (51.8+/-4.7 yrs), 2641 women aged 35-44 years (40.6+/-2.8 yrs), and 3584 women aged 45-60 years (51.4+/-4.4 yrs). Median (2.5th and 97.5th percentiles) for TSH (mU/l) were 1.52 (0.20-4.54) for men, 1.78 (0.22-5.54) for women aged 35-44 years, and 1.96 (0.22-6.80) for women aged 45-60 years. The TSH distribution of women was shifted to the right compared with men. Arithmetic mean fT4 (+/-SD) was 10.7+/-1.7 ng/l (13.8 +/-2.2 pmol/l) for men and 10.9+/-1.8 ng/l (14.0+/-2.3 pmol/l) for women. The prevalence of abnormal TSH values in men, and in women (35-44 yrs and 45-60 yrs) were TSH<0.4 mU/l 7.0%, 5.3% and 4.4%; TSH 4.0-9.9 mU/l 4.0%, 7.2% and 11.1% and TSH > or =10.0 mU/l 0.2%, 0.4% and 0.7%, respectively. Geometric mean serum TSH and arithmetic mean serum fT4 concentrations showed significant overall inter-regional differences for men and women (p<0.0001). There was also an inter-regional difference in the prevalence of thyroid dysfunction for men (p=0.003), and for the older group of women (i.e. > or =45 yrs) (p=0.04) exclusively. Over the age of 45 years, the women: men ratio for unrecognized elevated TSH levels (> or =4.0 mU/l) was 2.82, whereas it was 0.64 for low TSH levels (<0.4 mU/l). In summary, abnormal TSH values and thyroid dysfunction were more prevalent in women than men, increased with age and were significantly associated with environmental factors. A high prevalence of identified thyroid diseases in the French population was confirmed by the high number of subjects in this study with laboratory evidence of abnormal biochemical thyroid function. Further studies are needed to determine the geographical determinants of thyroid dysfunctions, especially regional differences in iodine intakes, and to assess the long-term adverse effects of biochemical thyroid dysfunction on all-cause morbidity.

Adult↗

PubMed1987

Immunoelectron microscopic demonstration of thyroglobulin and thyroid hormones in rat thyroid gland.

We have developed a post-embedding immunogold technique for electron microscopic localization and quantitation of thyroglobulin (TG), thyroxine (T4), and triiodothyronine (T3) in rat thyroid. Labeling for TG was located on rough endoplasmic reticulum, Golgi apparatus, exocytotic vesicles, luminal colloid, colloid droplets, and lysosomes, whereas labeling for thyroid hormones was located on luminal colloid, colloid droplets, and lysosomes. We tested different procedures of fixation, dehydration, embedding, polymerization, and immunoincubation to optimize ultrastructural preservation and immunolabeling. Fixation with glutaraldehyde and osmium was possible with retained antigenicity. Dehydration temperature and the choice of embedding resin were the two crucial factors for good immunolabeling. Low-temperature dehydration greatly improved immunolabeling and could be combined with embedding in the methacrylate LR White or the epoxide Agar 100 (equivalent of Epon 812) polymerized at 40-60 degrees C, as the temperature during subsequent embedding and polymerization was of little importance for the immunoreactivity. Labeling on LR White sections was always higher than on Agar 100 sections. Various etching procedures were tested without improved specific labeling. Etching with hydrochloric acid gave nonspecific labeling of certain cell compartments.

Animals↗

PubMed1991

Measurement of thyroid hormone in the rat thyroid gland by radioimmunoassay.

The present paper describes (i) a hydrolysis technique with Pronase and leucine aminopeptidase using one rat thyroid gland, resulting in maximum release of thyroid hormones and minimum deiodination, and (ii) a simple and rapid procedure for thyroid hormone radioimmunoassays in thyroid hydrolysates using commercial kits intended for serum thyroid hormone determinations. The procedure is used to determine T4, T3, and rT3 concentrations and hormonal molar ratios in a thyroid gland from a male Wistar rat. The reliability of the method is also studied.

Animals↗

PubMed1992

The unique C-termini of the thyroid hormone receptor variant, c-erbA alpha 2, and thyroid hormone receptor alpha 1 mediate different DNA-binding and heterodimerization properties.

Thyroid hormone receptors (TRs) mediate the regulation of gene transcription by thyroid hormone (T3) by binding to T3-responsive elements (TREs) in target genes. c-erbA alpha 2 is a C-terminal TR variant which does not bind T3 and is a dominant inhibitor of T3 action. When synthesized in Escherichia Coli, alpha 2 formed two TRE-binding complexes similar to the monomeric and homodimeric forms of TR alpha 1. However, alpha 2 did not bind nearly as well as TR alpha 1. Furthermore, alpha 2 failed to bind DNA with proteins that heterodimerized with TR alpha 1. TR alpha 1 and alpha 2 also did not bind DNA as heterodimers with one another. The differences between TR alpha 1 and alpha 2 were further analyzed by studying a variety of C-terminal mutants synthesized in reticulocyte lysates. Deletion of the last 20 of the 122 unique amino acids (aa) of alpha 2 increased its DNA binding to approximately the level of TR alpha 1, indicating that the C-terminus of alpha 2 is an inhibitory domain. This alpha 2 mutant (alpha 2 delta C) was still unable to heterodimerize with nuclear proteins, as were C-terminal deletion mutants of TR alpha 1. We hypothesized that fusion of TR alpha 1-specific sequences to the C-terminus of alpha 2 delta C would transfer the property of heterodimerization. Indeed, although alpha 2/alpha 1 chimeras containing the last 40 and 70 aa of TR alpha 1 failed to heterodimerize with nuclear proteins, addition of the last 100 or 150 aa of TR alpha 1 did render alpha 2 delta C heterodimerization competent. Thus, TR alpha 1 contains a C-terminal structure which is necessary for heterodimerization and can confer this property on alpha 2, which lacks this domain. The effects of the unique C-termini of TR alpha 1 and alpha 2 on their in vitro DNA binding have important implications for their mechanisms of action in vivo.

Amino Acid Sequence↗

PubMed2006

A family showing resistance to thyroid hormone associated with chronic thyroiditis and its clinical features: A case report.

Resistance to thyroid hormone (RTH) is characterized by decreased tissue responsiveness to thyroid hormone, due mainly to mutation of the thyroid hormone receptor (TR) beta gene. It has been reported that serum of patients with RTH lacks autoantibodies against thyroglobulin (Tg) and thyroid peroxidase (TPO), except in rare cases where there is co-occurrence of coincidental autoimmune thyroiditis. Here we describe the five-year medical history of a Japanese woman and her father with RTH and coincidental chronic thyroiditis. The woman, aged 28 years, was referred to our hospital because of suspected hyperthyroidism. She showed a normal level of TSH and elevated levels of free triiodothyronine (FT3) and free thyroxine (FT4). Anti-Tg and anti-TPO antibodies were slightly positive. Since RTH was suspected, her parents were investigated with informed consent. Her father showed elevated levels of TSH, FT3 and FT4, and was positive for both anti-Tg antibody and anti-TPO antibody. Her mother had hypothyroidism caused by chronic thyroiditis. Sequencing of the TR beta gene showed that the patient and her father had a codon 453 mutation resulting in a CCT (proline) to ACT (threonine) substitution. The patient gradually developed emotional disturbance, and was admitted to a psychiatry ward for two months, where she was treated with lorazepam and her condition improved. Her father, on the other hand, has been doing well for five years. The patient and the father showed different clinical courses, even though they carried the same mutation of the TR beta gene. The fact that the father showed an elevated TSH level, whereas the patient did not, was thought to be due to decreased thyroid function caused by chronic thyroiditis.

Adult↗

PubMed2006

Two uniquely arranged thyroid hormone response elements in the far upstream 5' flanking region confer direct thyroid hormone regulation to the murine cholesterol 7alpha hydroxylase gene.

Cholesterol 7alpha hydroxlyase (CYP7A1) is a key enzyme in cholesterol catabolism to bile acids and its activity is important for maintaining appropriate cholesterol levels. The murine CYP7A1 gene is highly inducible by thyroid hormone in vivo and there is an inverse relationship between thyroid hormone and serum cholesterol. Eventhough gene expression has been shown to be upregulated, whether the induction was mediated through a direct effect of thyroid hormone on the CYP7A1 promoter has never been established. Using gene targeted mice, we show that either of the two TR isoforms are sufficient to maintain normal hepatic CYP7A1 expression but a loss of both results in a significant decrease in expression. We also identified two new functional thyroid hormone receptor-binding sites in the CYP7A1 5' flanking sequence located 3 kb upstream from the transcription start site. One site is a DR-0, which is an unusual type of TR response element, and the other consists of only a single recognizable half site that is required for TR/retinoid X receptor (RXR) binding. These two independent TR-binding sites are closely spaced and both are required for full induction of the CYP7A1 promoter by thyroid hormone, although the DR-0 site was more crucial.

5' Flanking Region↗

PubMed1990

Calcium is the first messenger for the action of thyroid hormone at the level of the plasma membrane: first evidence for an acute effect of thyroid hormone on calcium uptake in the heart.

The thyroid hormone T3 produced a very rapid and transient increase in 45calcium uptake by freshly isolated rat heart slices, which was seen already 15 sec after the addition of the hormone, reached a maximum at 30 sec, and then progressively declined and returned to control values after 10 min. This effect of T3 was independent of extracellular calcium, concentration related (evident at a physiological concentration of 10 pM, reached maximum of about 75% above control at 1 nM, and was smaller at greater concentrations), and thyroid hormone specific, as judged from the order of potency of several thyroid hormone analogs: L-T3 greater than L-T4 greater than or equal to D-T3 greater than 3'-isopropyl-3,5-L-diiodothyronine greater than D-T4 greater than 3,5-L-diiodothyronine greater than r-L-T3 greater than D,L-thyronine. The inorganic calcium channel blockers La3+, Cd2+, and Mn2+ inhibited, in a concentration-related fashion, basal and T3-induced increases in 45Ca uptake in the cardiac slices. The organic calcium channel blockers verapamil, nifedipine, and diltiazem were without effect, indicating that in the quiescent cardiac slice the effect of T3 on 45Ca uptake is independent of sarcolemmal depolarization. Additional studies demonstrated that the stimulatory effect of T3 on 2-deoxyglucose uptake by the cardiac slices required extracellular calcium and was inhibited by the calcium channel blockers La3+, Cd2+, and Mn2+. The present study provides conclusive evidence for two central issues: that calcium is the first messenger for the prompt, plasma membrane-mediated action of thyroid hormone to increase cellular sugar uptake, and that thyroid hormone produces an acute increase in calcium uptake by the heart, an effect that is demonstrable at physiological concentrations and is thyroid hormone specific and, therefore, points to a physiological relevance for this action.

Animals↗

PubMed2006

Transactivation activity of thyroid hormone receptors in fish (Conger myriaster) in response to thyroid hormones.

We previously isolated cDNAs encoding conger eel (Conger myriaster) thyroid hormone (TH) receptors (TRs). In the present study, we investigated the transactivation activities of conger eel TRs treated with THs (3,3',5-triiodo-l-thyronine [T3], l-thyroxine [T4], and 3,3',5'-triiodo-l-thyronine [rT3]), or ligands and activators of other nuclear receptors. Following transient transfection into the Japanese eel (Anguilla japonica) hepatocyte cell line Hepa-E1, the conger eel TRs (cTRs) showed TH-dependent activation of transcription from a TH-responsive promoter. However, no transactivation activity of any of the four cTRs was observed with ligands or activators of other nuclear receptors. Although T3 activation for cTRs is stronger than other THs (T3>T4>rT3), the transactivation sensitivity was different from the activity of cTRs with THs, respectively. Therefore, we conclude that cTRs can act in concert with THs in fish metamorphosis.

Animals↗

PubMed1992

The role of selenium in thyroid hormone metabolism and effects of selenium deficiency on thyroid hormone and iodine metabolism.

Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases, which convert thyroxine (T4) to the more metabolically active 3,3'-5 triiodothyronine (T3). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [125I]N-bromoacetyl reverse triiodothyronine, is also labeled with 75Se by in vivo treatment of rats with 75Se-Na2SeO3. Thus, the type I iodothyronine 5'-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent selenium deficiency could be a major determinant of the severity of iodine deficiency.

Animals↗