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PubMed1981

The stimulation of thyroid hormone secretion in vitro by thyroid-stimulating antibodies.

A new simple technique is described for the in vitro assay of thyroid-stimulating antibody (TSAb) in serum. Thyroid slices are incubated with serum in two-compartmental dialysis pot, followed by measurement of the thyroid hormone concentration in the dialysis fluid by RIA. Heat-inactivated normal serum applied directly to the tissue has no effect on the basal level of response. A dose-dependent relationship is demonstrated for both TSH and TSAb. Serum from patients with untreated Graves' hyperthyroidism is clearly shown to stimulate thyroid hormone secretion. Porcine thyroid tissue has been used and responds well to TSAb. This technique not only has the advantage of simple methodology, but also reflects the biological activity of TSAb. Therefore it will prove useful for further studies of the significance of TSAb and the pathogenesis of Graves' disease.

Animals↗

PubMed1989

Incidence of thyroid hormone autoantibodies in patients with thyroid diseases with respect to diagnosis, other types of autoantibodies, duration of disease and treatment.

Thyroid hormone autoantibodies (THAA] were estimated in a total of 149 patients (139 women and 10 men) with various thyroid diseases. THAA were found in a total of 22 patients (all women), i.e. 14.7%. In 8 of them both T4Ab and T3Ab were found, while T4Ab only were found in 4 patients and T3Ab only in 10 patients. The highest incidence of THAA was found in patients with diffuse lymphocytic thyroiditis (i.e. 11 cases out of a total of 64 patients) and similarly high incidence was in patients with suspected autoimmune goiter but without thin needle biopsy (i.e. 5 cases out of a total of 21 patients). If only the patients with manifested or silent hypothyroidism were selected, T4Ab were found exclusively in this group, while the incidence of T3Ab was 3 times higher as that in patients without hypothyroidism. Though the incidence of T4Ab in patients with positive antithyroglobulin and antimicrosomal antibodies was 3 times higher than in negative ones, the difference was not significant. No correlation was found between the incidence of THAA on one hand and the duration of disease, the duration of treatment and the drug used for treatment on the other. However, a significant correlation was found between the incidence of THAA and the presence of goiter (P less than 0.05).

Autoantibodies↗

PubMed1992

Synergistic activation of the rat growth hormone promoter by Pit-1 and the thyroid hormone receptor.

The rat GH (rGH) gene is expressed in the pituitary in a highly tissue-specific manner. A pituitary-specific transcription factor, Pit-1 (or GHF-1), and other, more tissue-general factors, including the thyroid hormone receptor (T3R), are important for regulating rGH promoter activity. The relative roles of Pit-1, T3R, and protein kinases in the activation of the rGH promoter were studied. Each component was supplied individually or in combination with the others to human monocyte U937 cells. The transfected rGH promoter was inactive in these cells even when it was cotransfected with either Pit-1 or T3R expression vectors. The rGH promoter carried in a truncated pUC vector could be activated by expression of the T3R if the cells were cultured with inducers of protein kinase-A (forskolin) and protein kinase-C [phorbol 12-myristate 13-acetate (PMA)] activity. By contrast, the PMA- and forskolin-dependent activation of the rGH promoter by Pit-1 expression was comparatively insignificant unless 1) the sequences deleted from the pUC vector (including a putative site for the transcription factor AP1) were restored to the plasmid carrying the rGH promoter; or 2) the T3R was coexpressed, which led to a marked synergistic response. These results indicate the relative inactivity of Pit-1 in isolation from other factors. Activation by forskolin and PMA did not require de novo protein synthesis. The synergistic activation by Pit-1 and the T3R was enhanced, but was not dependent upon, thyroid hormone (T3). The T3-dependent effect operated predominately through a thyroid hormone response element located up-stream of the two Pit-1-binding sites within the rGH promoter, whereas the T3-independent effect did not require any of the known T3R-binding sites on the rGH promoter. These results suggest a role for the more tissue-general T3R and protein kinases in the activation of the rGH promoter. They demonstrate the synergistic interplay between the T3R and Pit-1, underscore the dependence of Pit-1 action on other transcription factors, and implicate Pit-1 as a cofactor, rather than the dominant factor, influencing the tissue-specific expression of the rGH promoter.

Animals↗

PubMed2006

A developmental switch induced by thyroid hormone: Xenopus laevis metamorphosis.

Thyroid hormone induces the complete metamorphosis of anuran tadpoles into juvenile frogs. Arguably, anuran metamorphosis is the most dramatic effect of a hormone in any vertebrate. Recent advances in pharmacology and molecular biology have made the study of this remarkable process in the frog Xenopus laevis attractive to developmental biologists and endocrinologists alike. In particular, the availability of a straightforward transgenesis assay and the near completion of the Xenopus tropicalis genome are enabling significant advances to be made in our understanding of the major remaining problems of metamorphosis: the extraordinary tissue specificity of responses, the precise timing of morphological changes, the degree of cell autonomy of hormone responses and developmental competence. We argue that X. laevis metamorphosis presents an exciting opportunity for understanding the role of thyroid hormone in vertebrate development.

Animals↗

PubMed1994

Hormone-nuclear receptor interactions in health and disease. Thyroid hormone resistance.

The syndromes of resistance to thyroid hormone (RTH) are rare disorders characterized by elevated levels of circulating free thyroid hormones, inappropriate TSH secretion and variably reduced peripheral tissue responses to iodothyronine action. On the basis of clinical features, two major forms of RTH are recognized: generalized resistance (GRTH) in which patients are asymptomatic with few clinical signs, and pituitary resistance (PRTH) where patients present with features associated with thyrotoxicosis. However, a review of the literature and our own experience indicates that there is a wide overlap of clinical and biochemical features between individuals with GRTH or PRTH. Genetic analysis shows that both disorders are associated with a number of different mutations in the thyroid hormone receptor beta (TR-beta) gene which localize to two regions in the hormone-binding domain. The mutant proteins are transcriptionally impaired but preserve the ability to bind DNA, dimerize and inhibit the function of their wild-type counterparts in a dominant negative manner. Dominant negative effects of mutant receptors within the pituitary-thyroid feedback axis generate abnormal thyroid function test results characteristic of RTH. The variable peripheral resistance may be related to differences in tissue distribution of TR-alpha versus TR-beta receptor isoforms, variable dominant negative effects of mutant receptors on different target genes or other factors not related to the receptor mutation. Although GRTH and PRTH represent the variable phenotypic spectrum of a single genetic entity, this clinical distinction will remain useful as a guide to appropriate treatment.

Diagnosis, Differential↗

PubMed1997

Plasma gonadotropin II, sex steroids, and thyroid hormones in wild striped bass (Morone saxatilis) during spermiation and final oocyte maturation.

The blood levels of gonadotropin II (GtH II), sex-steroid hormones, and thyroid hormones were determined in wild spermiating male striped bass (Morone saxatilis) in males and in females at various stages of final oocyte maturation (FOM), captured on their spawning grounds. The progression of spermiation was associated with increases in plasma GtH II and decreases in plasma testosterone (T), 11-ketotestosterone, and thyroxine (T4). Plasma triiodothyronine (T3) remained at high and relatively unchanged levels. Plasma levels of 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P) and 17,20beta, 21-trihydroxy-4-pregnen-3-one (17,20beta,21-P), the proposed maturation-inducing steroids (MIS) in striped bass, were low and unchanged during the same period. It was concluded that low progestogen levels are adequate to induce spermiation in striped bass, and that higher levels may be associated with spawning behavior. In the females, based on the profiles of the studied hormones, FOM was separated into two phases. Early FOM, which included germinal vesicle (GV) migration and lipid-droplet coalescence, was associated with elevations in plasma GtH II, T, and estradiol 17beta. Late FOM, which included GV breakdown and yolk-globule coalescence, was associated with a further surge in plasma GtH II, increases in the levels of the two MIS, mainly 17, 20beta-P, and a drop in T4. Plasma T3 levels did not change during FOM. Examination of conjugated steroids demonstrated, in the males, a reduction in conjugated androgens at the peak of the spawning season and, in the females, a small increase in conjugated 17, 20beta-dihydroxylated and 5beta-reduced,3alpha-hydroxylated steroids after spawning. This is the most comprehensive report, to date, on the endocrine regulation of gonadal maturation in wild striped bass, demonstrating that a two-stage process of FOM is regulated by different endocrine signals, providing further evidence for the involvement of 17,20beta-P as a MIS in the females, and indicating that both males and females are in an euthyroid state during the spawning season.

Animals↗

PubMed1980

[Effect of thyrotropic hormone on the membrane potential of thyroid gland cells and thyroid hormone secretion with aging].

Effect of thyrotropic hormone (TTH) on membrane potential (MP) of thyroid cells and thyroid hormone secretion was studied in experiments on male rats of two age groups (7--12- and 27--32-month-old animals). It was found that during the first 3 hours after TTH administration (5 U/100 g i. v.) the depolarization of secretory cell membranes of adult rats was done pronounced and developed more rapidly than in old ones and that an increase in free thyroxin (T4) correlation with MP changes with time. In a dose of 0.5 U/100 g TTH caused a significant rise in T4 secretion only in old rats. The cAMP level in the thyroid gland declined with aging. In a dose of 5 U/100 g TTH provoked a significant increase in the cAMP content in adult rats and had no effect on its content in old ones. A relationship between the MP level of thyroid secretory cells and thyroid hormone secretion is discussed.

Age Factors↗

PubMedDate not supplied

A c-erb-A binding site in rat growth hormone gene mediates trans-activation by thyroid hormone.

The substance 3,5,3-triiodothyronine (T3) stimulates growth hormone gene transcription in rat pituitary tumour cells. This stimulation is thought to be mediated by the binding of nuclear T3 receptors to regulatory elements 5' to the transcriptional start site. Understanding of the mechanism by which thyroid hormone activates gene transcription has been limited by failure to purify nuclear T3 receptors because of their low abundance, and by the absence of defined T3 receptor-DNA binding sites affecting T3 regulation. Recently, human and avian c-erb-A gene products have been shown to bind thyroid hormone with high affinity and to have a molecular weight and nuclear association characteristic of the thyroid hormone receptor. In the present report, we describe the development of an avidin-biotin complex DNA-binding assay which can detect specific, high-affinity binding of rat pituitary cell T3 receptors to the sequence 5'CAGGGACGTGACCGCA3', located 164 base pairs 5' to the transcriptional start site of the rat growth hormone gene. An oligonucleotide containing this sequence transferred T3 regulation to the herpes simplex virus thymidine kinase promoter in transfected rat pituitary GC2 cells, and specifically bound an in vitro translation product of the human placental c-erb-A gene. The data provide supporting evidence that the human c-erb-A gene product mediates the transcriptional effects of T3 and also that GC2 cell nuclear extracts contain additional factors that modify the binding of pituitary T3 receptors to the rat growth hormone gene T3 response element.

Animals↗

PubMed1987

Transport of p-aminohippurate in renal cortical slices of rats of different ages following treatment with thyroid hormones.

Following treatment with thyroid hormones PAH accumulation is increased in renal cortical slices of 5-, 10-, 20-, 30-, 50- and 105-day-old rats. Both thyroid hormones are more effective in young than in adult rats. A single dose of T3 or T4 (20 micrograms/100 g b.m.) administered 24 h before measurement is effective whereas acute effects of T3 or T4 on PAH transport could not be demonstrated. Treatment with thyroid hormones (20 micrograms/100 g b.m., 3 days, once a day) is without any influence on body mass; there is a tendency to an increase of kidney mass following treatment with T3 or T4. Simultaneous administration of an inhibitor of protein biosynthesis (neomycin, 1 or 5 mg/100 g b.m.) reduces the effect of T3 treatment. An additional low dose of T3, 24 h before measurement of PAH transport can restore the effect of T3 treatment which was performed 9 days before.

Aminohippuric Acids↗

PubMed1992

A point mutation of the T3 receptor beta 1 gene in a kindred of generalized resistance to thyroid hormone.

Mutations of the thyroid hormone receptor (TR) beta 1 gene have recently been detected in several unrelated families with generalized resistance to thyroid hormone (GRTH). We now report a novel point mutation in the TR beta 1 gene in a case of a Korean-Japanese kindred. The intracellular localization and the amount of TR proteins were considered to be normal by the immunocytochemical study of cultured skin fibroblasts from the patients using anti-T3 receptor antibody. The cDNA of the T3-binding domain of the TR beta 1 gene, synthesized from the total RNA of the patients' fibroblasts, was amplified by the polymerase chain reaction, and was sequenced. A point mutation, A to G, in one allele at 1612 resulting in an amino acid substitution from lysine 438 to glutamic acid was detected. The same mutation was identified in one allele in each of the affected members. In vitro translation products of the mutant TR beta 1 gene showed decreased T3-binding activity. These data suggest that a TR mutation is predominantly responsible for GRTH, irrespective of ethnic background.

Adolescent↗

PubMed2005

Insulin sensitivity and counter-regulatory hormones in hypothyroidism and during thyroid hormone replacement therapy.

We examined insulin sensitivity and secretion, together with the levels of selected glucoregulatory hormones, in 15 female patients with severe hypothyroidism (H) and during subsequent thyroid hormone replacement therapy (HRT) using the euglycaemic hyperinsulinaemic clamp technique. Insulin action, as evaluated by glucose disposal, the insulin sensitivity index, and fasting post-hepatic insulin delivery rate were established. The basal levels of insulin, C-peptide and counter-regulatory hormones were measured in basal condition. In H, glucose disposal (p<0.01), the insulin sensitivity index (p<0.01) and post-hepatic insulin delivery rate (p<0.05) were significantly lower than during HRT. No significant changes in the levels of fasting insulin and C-peptide were observed. The levels of counter-regulatory hormones in patients with H were significantly higher than during HRT (glucagon, p<0.05; epinephrine, p<0.01; cortisol, p<0.05; growth hormone, p<0.05). In H, an inverse correlation between insulin sensitivity and insulin secretion was observed (p<0.05). Cortisol was the most important factor affecting the variability of insulin sensitivity values, regardless of thyroid function (p=0.0012). In conclusion, H altered both insulin sensitivity and the levels of selected counter-regulatory hormones. The situation was restored by HRT, as manifested not only by normalisation of insulin sensitivity, secretion and levels of glucoregulatory hormones, but also by improvement of their relationships.

Adult↗

PubMed1983

Effects of hysterectomy and uterine extracts on growth hormone, somatomedin, prolactin, thyrotrophin and thyroid hormones in adult rats.

Plasma concentrations and anterior pituitary content of growth hormone (rGH), thyroid stimulating hormone (rTSH), and rat prolactin (rPrl) as well as the plasma concentrations of triiodothyronine (T3), thyroxine (T4) and somatomedin A (SM-A) have been determined in intact, castrated or hysterectomized adult rats with and without treatment with steroid-free, crude uterine extracts. Hysterectomy caused a significant increase in the plasma GH but decrease in the plasma TSH concentrations. Injection of crude, steroid-free uterine extracts for 14 days had the following effects: decreased plasma GH concentration of intact rat and anterior pituitary GH content of both intact and castrated animals; increased plasma TSH and T3 concentrations above the ovariectomized control; decreased pituitary content of prolactin in castrated rats. The plasma levels of immunoreactive somatomedins A were negatively correlated to the plasma GH concentrations but positively correlated to the body weight. It was concluded that the uterus is not only a target for different endocrine influences but contains biologically active, non-steroidal substances which have a complex effect on the endocrine system of adult, female rats.

Animals↗

PubMed2004

[The molecular and structural effects of thyroid hormone in bones].

During development, thyroid hormone deficiency results in delayed skeletal maturation and epiphyseal dysgenesis, resulting in reduced growth and skeletal abnormalities. Thyroid hormone also has effects on bones of adults. Thyrotoxicosis is frequently associated with increased bone turnover and decreased bone mass. However, the mechanisms that mediate its effects on bone tissue are poorly understood. Thyroid hormone acts indirectly in the skeleton, by increasing the secretion of growth hormone and insulin-like growth factor-1; or directly, by modulating target genes via specific nuclear receptors. In vitro findings, such as the presence of thyroid receptors (TRs) and the induction of genes and proteins in skeletal cells by thyroid hormone, emphasize the importance of direct actions. The aim of this review is to summarize the in vivo and in vitro findings related to the effects of thyroid hormone on the skeleton.

Bone Development↗

PubMed1997

Identification of a nuclear protein from rat developing brain as heterodimerization partner with thyroid hormone receptor-beta.

Thyroid hormone receptors (TR) are ligand-activated transcription factors that modulate the expression of certain target genes in a developmental and tissue-specific manner. These specificities are determined by the tissue distribution of the TR isoforms alpha1 and beta1, the structure of the thyroid hormone response element (TRE) bound by the receptor, and heterodimerization partners. Among these, retinoid X receptors (RXR) have been recognized as the principal partners for TR. The present work reports the identification of a novel nuclear protein from 19-day-old embryonic rat brain that displays a distinct interaction pattern with TR isoforms at the level of the TRE of two genes known to be differentially expressed and regulated by thyroid hormone (T3): the ubiquitous malic enzyme and the brain-specific myelin basic protein. Electrophoretic gel mobility shift assays demonstrate that only TRbeta1 forms a specific complex with the rat brain nuclear factor on the myelin basic protein-TRE, but not on the malic enzyme-TRE. Thus, the interaction is selectively determined by both the receptor isoform and the structure of the TRE. The expression of this brain nuclear factor is restricted to the perinatal period, when myelination is sensitive to T3. Gel supershift assays with RXR-specific antibodies indicate that this factor is not one of the known RXR isoforms. However, it is most likely a new member of the RXR subfamily because it could be supershifted with an antibody raised against the highly conserved DNA-binding domain of RXRs.

Animals↗

PubMed2006

[Thyroid hormone and the cardiovascular system].

Thyroid hormone has many effects on the heart and vascular system. Many of the clinical manifestations of hyperthyroidism are due to the ability of thyroid hormone to alter cardiovascular hemodynamics. The hemodynamic effects of hypothyroidism are opposite to those of hyperthyroidism, although the clinical manifestations are less obvious. This review will integrate what is known about the mechanisms of thyroid hormone action on the heart with recent observations from both experimental and clinical studies of hyperthyroidism and hypothyroidism. Thyroid hormone has both direct and indirect actions on the cardiovascular system. Patients with thyroid disease, especially those with hyperthyroidism, often have symptoms and signs indicating changes in cardiovascular hemodynamics. Indeed, symptoms and signs referable to the cardiovascular system may be the only manifestations of thyroid dysfunction, and thyroid function should therefore be assessed by the measurement of serum thyrotropin concentrations in all patients with cardiovascular disease. Some suggest that the administration of triiodothyronine may benefit some patients with cardiovascular disease.

Animals↗

PubMed1986

Alteration of lymphocyte reactivities by thyroid hormones.

The effects of thyroid hormones (L-T4, L-T3 and rT3) on the proliferative response of rabbit peripheral blood lymphocytes to T-cell mitogens, PHA and Con A, and B cell specific goat anti-rabbit light chain antibodies (Anti-L) were investigated. It was observed that L-T4 potentiated the lymphocyte response to mitogens and Anti-L in a dose-dependent manner: 10(-9) M and 10(-8) M had no effect while 10(-7)-10(-5) M significantly enhanced the lymphocyte response. L-T3 (10(-11)-10(-8) M) had no effect on the lymphocyte response to PHA and Con A. At 10(-7) M, L-T3 inhibited the response to PHA but not Con A. L-T3 (10(-11)-10(-7) M) suppressed the lymphocyte response to Anti-L. The suppression was directly proportional to the L-T3 concentration. rT3 (10(-11)-10(-7) M) inhibited the proliferative response to PHA and Anti-L in a dose-related manner. Its effect on the lymphocyte response to Con A was stimulatory at 10(-11) M but inhibitory at higher concentrations (10(-8) and 10(-7) M). rT3 suppressed the enhancement by L-T4 of the lymphocyte response to the mitogens and Anti-L. The degree of suppression was proportional to its concentration. This data indicated that thyroid hormones can alter the reactivities of lymphocytes. The direction and magnitude of the alteration appear to depend on the concentration of a specific thyroid hormone encountered by the responding cells.

Adjuvants, Immunologic↗

PubMed2006

Thyroid hormone and the growth plate.

Thyroid hormone was first identified as a potent regulator of skeletal maturation at the growth plate more than forty years ago. Since that time, many in vitro and in vivo studies have confirmed that thyroid hormone regulates the critical transition between cell proliferation and terminal differentiation in the growth plate, specifically the maturation of growth plate chondrocytes into hypertrophic cells. However these studies have neither identified the molecular mechanisms involved in the regulation of skeletal maturation by thyroid hormone, nor demonstrated how the systemic actions of thyroid hormone interface with the local regulatory milieu of the growth plate. This article will review our current understanding of the role of thyroid hormone in regulating the process of endochondral ossification at the growth plate, as well as what is currently known about the molecular mechanisms involved in this regulation.

Animals↗

PubMed2003

Identification of monocarboxylate transporter 8 as a specific thyroid hormone transporter.

Transport of thyroid hormone across the cell membrane is required for its action and metabolism. Recently, a T-type amino acid transporter was cloned which transports aromatic amino acids but not iodothyronines. This transporter belongs to the monocarboxylate transporter (MCT) family and is most homologous with MCT8 (SLC16A2). Therefore, we cloned rat MCT8 and tested it for thyroid hormone transport in Xenopus laevis oocytes. Oocytes were injected with rat MCT8 cRNA, and after 3 days immunofluorescence microscopy demonstrated expression of the protein at the plasma membrane. MCT8 cRNA induced an approximately 10-fold increase in uptake of 10 nM 125I-labeled thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3) and 3,3'-diiodothyronine. Because of the rapid uptake of the ligands, transport was only linear with time for <4 min. MCT8 did not transport Leu, Phe, Trp, or Tyr. [125I]T4 transport was strongly inhibited by L-T4, D-T4, L-T3, D-T3, 3,3',5-triiodothyroacetic acid, N-bromoacetyl-T3, and bromosulfophthalein. T3 transport was less affected by these inhibitors. Iodothyronine uptake in uninjected oocytes was reduced by albumin, but the stimulation induced by MCT8 was markedly increased. Saturation analysis provided apparent Km values of 2-5 microM for T4, T3, and rT3. Immunohistochemistry showed high expression in liver, kidney, brain, and heart. In conclusion, we have identified MCT8 as a very active and specific thyroid hormone transporter.

Amino Acid Sequence↗