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1
Cordeiro, Aline, Luana Lopes Souza, Marcelo Einicker-Lamas, and Carmen Cabanelas Pazos-Moura. "Non-classic thyroid hormone signalling involved in hepatic lipid metabolism." Journal of Endocrinology 216, no. 3 (January 7, 2013): R47—R57. http://dx.doi.org/10.1530/joe-12-0542.
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Thyroid hormones are important modulators of lipid metabolism because the liver is a primary hormonal target. The hypolipidaemic effects of thyroid hormones result from the balance between direct and indirect actions resulting in stimulation of lipid synthesis and lipid oxidation, which favours degradation pathways. Originally, it was believed that thyroid hormone activity was only transduced by alteration of gene transcription mediated by the nuclear receptor thyroid hormone receptors, comprising the classic action of thyroid hormone. However, the discovery of other effects independent of this classic mechanism characterised a new model of thyroid hormone action, the non-classic mechanism that involves other signalling pathways. To date, this mechanism and its relevance have been intensively described. Considering the increasing evidence for non-classic signalling of thyroid hormones and the major influence of these hormones in the regulation of lipid metabolism, we reviewed the role of thyroid hormone in cytosolic signalling cascades, focusing on the regulation of second messengers, and the activity of effector proteins and the implication of these mechanisms on the control of hepatic lipid metabolism.
2
Yu, Jing, Siyi Shen, Ying Yan, Lingxiao Liu, Rongkui Luo, Shengnan Liu, Yuting Wu, Yuying Li, Jingjing Jiang, and Hao Ying. "Iodide Excess Inhibits Thyroid Hormone Synthesis Pathway Involving XBP1-Mediated Regulation." Nutrients 15, no. 4 (February 9, 2023): 887. http://dx.doi.org/10.3390/nu15040887.
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Iodine is an essential micronutrient for producing thyroid hormone (TH); however, iodide excess can lead to adverse thyroidal effects. Unfortunately, the lack of a proper in vitro model system hampered the studies of the effect of iodide excess on thyroid physiology and pathology. Here, we demonstrated that excessive iodide intake downregulated the genes related to TH synthesis in the thyroids of mice. Since sodium iodide has no effect on these genes in cultured cell lines, we developed a three-dimensional (3D) culture system to enable the murine thyrocytes to form organoids in vitro with thyroid follicle-like structures and function and found that the in vivo effect of iodide excess could be mimicked in these thyroid organoids. Our data indicate that iodide excess mainly activated the XBP1-mediated unfolded protein response in both murine thyroid and thyroid organoids, while activation of XBP1 was able to mimic the sodium iodide effect on genes for the synthesis of TH in murine thyroid organoids. Lastly, our results suggest that XBP1 might transcriptionally repress the genes involved in the synthesis of TH. Based on these findings, we propose that iodide excess inhibits the transcription of genes related to TH synthesis through a mechanism involving XBP1-mediated action.
3
Köhrle, Josef. "Selenium, Iodine and Iron–Essential Trace Elements for Thyroid Hormone Synthesis and Metabolism." International Journal of Molecular Sciences 24, no. 4 (February 8, 2023): 3393. http://dx.doi.org/10.3390/ijms24043393.
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The adequate availability and metabolism of three essential trace elements, iodine, selenium and iron, provide the basic requirements for the function and action of the thyroid hormone system in humans, vertebrate animals and their evolutionary precursors. Selenocysteine-containing proteins convey both cellular protection along with H2O2-dependent biosynthesis and the deiodinase-mediated (in-)activation of thyroid hormones, which is critical for their receptor-mediated mechanism of cellular action. Disbalances between the thyroidal content of these elements challenge the negative feedback regulation of the hypothalamus–pituitary–thyroid periphery axis, causing or facilitating common diseases related to disturbed thyroid hormone status such as autoimmune thyroid disease and metabolic disorders. Iodide is accumulated by the sodium-iodide-symporter NIS, and oxidized and incorporated into thyroglobulin by the hemoprotein thyroperoxidase, which requires local H2O2 as cofactor. The latter is generated by the dual oxidase system organized as ‘thyroxisome’ at the surface of the apical membrane facing the colloidal lumen of the thyroid follicles. Various selenoproteins expressed in thyrocytes defend the follicular structure and function against life-long exposure to H2O2 and reactive oxygen species derived therefrom. The pituitary hormone thyrotropin (TSH) stimulates all processes required for thyroid hormone synthesis and secretion and regulates thyrocyte growth, differentiation and function. Worldwide deficiencies of nutritional iodine, selenium and iron supply and the resulting endemic diseases are preventable with educational, societal and political measures.
4
Ludgate, Marian. "Extrathyroidal thyroid hormone synthesis?" Journal of Endocrinology 210, no. 1 (May 3, 2011): 3–4. http://dx.doi.org/10.1530/joe-11-0159.
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A paper published in this issue of the Journal of Endocrinology has revisited the hypothesis that thyroid hormones may be generated by tissues outside the thyroid gland in higher organisms including mammals. This commentary appraises the strengths and weaknesses of the study, the alternative explanations for the findings and possible future measures to investigate further. The concept of extrathyroidal thyroxine and triiodothyronine synthesis has previously been proposed; by assuming that Nagao et al. and earlier authors are correct, the plausibility and possible mechanisms underlying the hypothesis are discussed.
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Sousa, J. C., G. Morreale de Escobar, P. Oliveira, M. J. Saraiva, and J. A. Palha. "Transthyretin is not necessary for thyroid hormone metabolism in conditions of increased hormone demand." Journal of Endocrinology 187, no. 2 (November 2005): 257–66. http://dx.doi.org/10.1677/joe.1.06406.
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Thyroid hormones circulate in blood mainly bound to plasma proteins. Transthyretin is the major thyroxine plasma carrier in mice. Studies in transthyretin-null mice revealed that the absence of transthyretin results in euthyroid hypothyroxinemia and normal thyroid hormone tissue distribution, with the exception of the choroid plexus in the brain. Therefore, transthyretin does not influence normal thyroid hormone homeostasis under standard laboratory conditions. To investigate if transthyretin has a buffer/storage role we challenged transthyretin-null and wild-type mice with conditions of increased hormone demand: (i) exposure to cold, which elicits thermogenesis, a process that requires thyroid hormones; and (ii) thyroidectomy, which abolishes thyroid hormone synthesis and secretion and induces severe hypothyroidism. Transthyretin-null mice responded as the wild-type both to changes induced by stressful events, namely in body weight, food intake and thyroid hormone tissue content, and in the mRNA levels of genes whose expression is altered in such conditions. These results clearly exclude a role for transthyretin in thyroid hormone homeostasis even under conditions of increased hormone demand.
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Severo, Juliana Soares, Jennifer Beatriz Silva Morais, Taynáh Emannuelle Coelho de Freitas, Ana Letícia Pereira Andrade, Mayara Monte Feitosa, Larissa Cristina Fontenelle, Ana Raquel Soares de Oliveira, Kyria Jayanne Clímaco Cruz, and Dilina do Nascimento Marreiro. "The Role of Zinc in Thyroid Hormones Metabolism." International Journal for Vitamin and Nutrition Research 89, no. 1-2 (July 2019): 80–88. http://dx.doi.org/10.1024/0300-9831/a000262.
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Abstract. Thyroid hormones play an important role in body homeostasis by facilitating metabolism of lipids and glucose, regulating metabolic adaptations, responding to changes in energy intake, and controlling thermogenesis. Proper metabolism and action of these hormones requires the participation of various nutrients. Among them is zinc, whose interaction with thyroid hormones is complex. It is known to regulate both the synthesis and mechanism of action of these hormones. In the present review, we aim to shed light on the regulatory effects of zinc on thyroid hormones. Scientific evidence shows that zinc plays a key role in the metabolism of thyroid hormones, specifically by regulating deiodinases enzymes activity, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) synthesis, as well as by modulating the structures of essential transcription factors involved in the synthesis of thyroid hormones. Serum concentrations of zinc also appear to influence the levels of serum T3, T4 and TSH. In addition, studies have shown that Zinc transporters (ZnTs) are present in the hypothalamus, pituitary and thyroid, but their functions remain unknown. Therefore, it is important to further investigate the roles of zinc in regulation of thyroid hormones metabolism, and their importance in the treatment of several diseases associated with thyroid gland dysfunction.
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Yaglova, Nataliya V., Sergey S. Obernikhin, Ekaterina P. Timokhina, Valentin V. Yaglov, Dibakhan A. Tsomartova, Svetlana V. Nazimova, Elina S. Tsomartova, Marina Y. Ivanova, Elizaveta V. Chereshneva, and Tatiana A. Lomanovskaya. "Bilateral Shifts in Deuterium Supply Similarly Change Physiology of the Pituitary–Thyroid Axis, but Differentially Influence Na+/I− Symporter Production." International Journal of Molecular Sciences 24, no. 7 (April 6, 2023): 6803. http://dx.doi.org/10.3390/ijms24076803.
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Deuterium, a stable isotope of hydrogen, is abundant in organisms. It is known to produce various biological effects. However, its impact in thyroid hormone synthesis and secretion is poorly studied. The aim of this investigation was to evaluate the dynamics of thyroid hormones and pituitary thyroid-stimulating hormone secretion during bilateral shifts in deuterium supply and assess a possible role of the Na+/I− symporter (NIS), the main iodide transporter, in altered thyroid function. The experiment was performed on adult male Wistar rats, which consumed deuterium-depleted ([D] = 10 ppm) and deuterium-enriched ([D] = 500,000 ppm) water for 21 days. The assessment of total thyroxine and triiodothyronine and their free fractions, as well as thyroid-stimulating hormone in blood serum, revealed the rapid response of the thyroid gland to shifts in the deuterium/protium balance. The present investigation shows that the bilateral changes in the deuterium body content similarly modulate thyroid hormone production and functional activity of the pituitary gland, but the responses of the thyroid and pituitary glands differ. The response of the thyroid cells was to increase the synthesis of the hormones and the pituitary thyrotropes, in order to reduce the production of the thyroid-stimulating hormone. The evaluation of NIS serum levels found a gradual increase in the rats that consumed deuterium-enriched water and no differences in the group exposed to deuterium depletion. NIS levels in both groups did not correlate with thyroid hormones and pituitary thyroid-stimulating hormone production. The data obtained show that thyroid gland has a higher sensitivity to shifts in the deuterium body content than the hypothalamic–pituitary complex, which responded later but similarly in the case of deuteration or deuterium depletion. It indicates a different sensitivity of the endocrine glands to alterations in deuterium content. It suggests that thyroid hormone production rate may depend on deuterium blood/tissue and cytosol/organelle gradients, which possibly disturb the secretory process independently of the NIS.
8
Fokina, E. A., and A. O. Shpakov. "Thyroid diseases and new approaches for their treatment." Siberian Journal of Clinical and Experimental Medicine 37, no. 3 (October 20, 2022): 90–97. http://dx.doi.org/10.29001/2073-8552-2022-37-3-90-97.
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The prevalence of thyroid diseases including autoimmune hyperthyroidism (Graves’ disease), autoimmune thyroiditis, and diff erent forms of thyroid cancer is increasing every year, while the eff ectiveness of their treatment remains low and is limited, mainly, to replacement therapy with thyroid hormones and surgical and radioisotope methods. This review presents the current state of the problem of pharmacological correction in thyroid diseases including new approaches to the regulation of the functional activity of the components of the thyroid hormone synthesis system in thyroid follicular cells, in particular, its initial, sensory component, the thyroid-stimulating hormone receptor. Among the drugs that are currently being developed, it is necessary to focus on allosteric regulators of the thyroid-stimulating hormone receptor, specifi c antibodies to it, as well as selective agonists of the β-isoform of thyroid hormone receptors.
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ROOT, Allen W., Dorothy SHULMAN, Jennifer ROOT, and Frank DIAMOND. "The interrelationships of thyroid and growth hormones: effect of growth hormone releasing hormone in hypo- and hyperthyroid male rats." Acta Endocrinologica 113, no. 4_Suppl (December 1986): S367—S375. http://dx.doi.org/10.1530/acta.0.112s367.
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ABSTRACT Growth hormone (GH) and the thyroid hormones interact in the hypothalamus, pituitary and peripheral tissues. Thyroid hormone exerts a permissive effect upon the anabolic and metabolic effects of GH, and increases pituitary synthesis of this protein hormone. GH depresses the secretion of thyrotropin and the thyroid hormones and increases the peripheral conversion of thyroxine to triiodothyronine. In the adult male rat experimental hypothyroidism produced by ingestion of propylthiouracil depresses the GH secretory response to GH-releasing hormone in vivo and in vitro, reflecting the lowered pituitary stores of GH in the hypothyroid state. Short term administration of large amounts of thyroxine with induction of the hyperthyroid state does not affect the in vivo GH secretory response to GH-releasing hormone in this animal.
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Gilbert, Mary E., Katherine L. O’Shaughnessy, Susan E. Thomas, Cal Riutta, Carmen R. Wood, Alicia Smith, Wendy O. Oshiro, et al. "Thyroid Disruptors: Extrathyroidal Sites of Chemical Action and Neurodevelopmental Outcome—An Examination Using Triclosan and Perfluorohexane Sulfonate." Toxicological Sciences 183, no. 1 (July 16, 2021): 195–213. http://dx.doi.org/10.1093/toxsci/kfab080.
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Abstract Many xenobiotics are identified as potential thyroid disruptors due to their action to reduce circulating levels of thyroid hormone, most notably thyroxine (T4). Developmental neurotoxicity is a primary concern for thyroid disrupting chemicals yet correlating the impact of chemically induced changes in serum T4 to perturbed brain development remains elusive. A number of thyroid-specific neurodevelopmental assays have been proposed, based largely on the model thyroid hormone synthesis inhibitor propylthiouracil (PTU). This study examined whether thyroid disrupting chemicals acting distinct from synthesis inhibition would result in the same alterations in brain as expected with PTU. The perfluoroalkyl substance perfluorohexane sulfonate (50 mg/kg/day) and the antimicrobial Triclosan (300 mg/kg/day) were administered to pregnant rats from gestational day 6 to postnatal day (PN) 21, and a number of PTU-defined assays for neurotoxicity evaluated. Both chemicals reduced serum T4 but did not increase thyroid stimulating hormone. Both chemicals increased expression of hepatic metabolism genes, while thyroid hormone-responsive genes in the liver, thyroid gland, and brain were largely unchanged. Brain tissue T4 was reduced in newborns, but despite persistent T4 reductions in serum, had recovered in the PN6 pup brain. Neither treatment resulted in a low dose PTU-like phenotype in either brain morphology or neurobehavior, raising questions for the interpretation of serum biomarkers in regulatory toxicology. They further suggest that reliance on serum hormones as prescriptive of specific neurodevelopmental outcomes may be too simplistic and to understand thyroid-mediated neurotoxicity we must expand our thinking beyond that which follows thyroid hormone synthesis inhibition.
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Liu, L., and TE Porter. "Endogenous thyroid hormones modulate pituitary somatotroph differentiation during chicken embryonic development." Journal of Endocrinology 180, no. 1 (January 1, 2004): 45–53. http://dx.doi.org/10.1677/joe.0.1800045.
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Growth hormone cell differentiation normally occurs between day 14 and day 16 of chicken embryonic development. We reported previously that corticosterone (CORT) could induce somatotroph differentiation in vitro and in vivo and that thyroid hormones could act in combination with CORT to further augment the abundance of somatotrophs in vitro. The objective of the present study was to test our hypothesis that endogenous thyroid hormones regulate the abundance of somatotrophs during chicken embryonic development. Plasma samples were collected on embryonic day (e) 9-14. We found that plasma CORT and thyroid hormone levels increased progressively in mid-embryogenesis to e 13 or e 14, immediately before normal somatotroph differentiation. Administration of thyroxine (T4) and triiodothyronine (T3) into the albumen of fertile eggs on e 11 increased somatotroph proportions prematurely on e 13 in the developing chick embryos in vivo. Furthermore, administration of methimazole, the thyroid hormone synthesis inhibitor, on e 9 inhibited somatotroph differentiation in vivo, as assessed on e 14; this suppression was completely reversed by T3 replacement on e 11. Since we reported that T3 alone was ineffective in vitro, we interpret these findings to indicate that the effects of treatments in vivo were due to interactions with endogenous glucocorticoids. These results indicate that treatment with exogenous thyroid hormones can modulate somatotroph abundance and that endogenous thyroid hormone synthesis likely contributes to normal somatotroph differentiation.
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Niedziela, Marek. "Hyperthyroidism in adolescents." Endocrine Connections 10, no. 11 (November 1, 2021): R279—R292. http://dx.doi.org/10.1530/ec-21-0191.
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The term 'hyperthyroidism' refers to a form of thyrotoxicosis due to inappropriate high synthesis and secretion of thyroid hormone(s) by the thyroid. The leading cause of hyperthyroidism in adolescents is Graves’ disease (GD); however, one should also consider other potential causes, such as toxic nodular goitre (single or multinodular), and other rare disorders leading to excessive production and release of thyroid hormones. The term 'thyrotoxicosis' refers to a clinical state resulting from inappropriate high thyroid hormone action in tissues, generally due to inappropriate high tissue thyroid hormone levels. Thyrotoxicosis is a condition with multiple aetiologies, manifestations, and potential modes of therapy. By definition, the extrathyroidal sources of excessive amounts of thyroid hormones, such as iatrogenic thyrotoxicosis, factitious ingestion of thyroid hormone, or struma ovarii, do not include hyperthyroidism. The aetiology of hyperthyroidism/and thyrotoxicosis should be determined. Although the diagnosis is apparent based on the clinical presentation and initial biochemical evaluation, additional diagnostic testing is indicated. This testing should include: (1) measurement of thyroid-stimulating hormone receptor (TSHR) antibodies (TRAb); (2) analysis of thyroidal echogenicity and blood flow on ultrasonography; or (3) determination of radioactive iodine uptake (RAIU). A 123I or 99mTc pertechnetate scan is recommended when the clinical presentation suggests toxic nodular goitre. A question arises regarding whether diagnostic workup and treatment (antithyroid drugs, radioiodine, surgery, and others) should be the same in children and adolescents as in adults, as well as whether there are the same goals of treatment in adolescents as in adults, in female patients vs in male patients, and in reproductive or in postreproductive age. In this aspect, different treatment modalities might be preferred to achieve euthyroidism and to avoid potential risks from the treatment. The vast majority of patients with thyroid disorders require life-long treatment; therefore, the collaboration of different specialists is warranted to achieve these goals and improve patients’ quality of life.
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Duthoit, Christine, Valérie Estienne, Frédéric Delom, Josée-Martine Durand-Gorde, Bernard Mallet, Pierre Carayon, and Jean Ruf. "Production of Immunoreactive Thyroglobulin C-Terminal Fragments during Thyroid Hormone Synthesis." Endocrinology 141, no. 7 (July 1, 2000): 2518–25. http://dx.doi.org/10.1210/endo.141.7.7573.
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Here, we studied the fragmentation of the prothyroid hormone, thyroglobulin (Tg), which occurs during thyroid hormone synthesis, a process which involves iodide, thyroperoxidase, and the H2O2-generating system, consisting of glucose and glucose oxidase. Various peptides were found to be immunoreactive to autoantibodies to Tg from patients and monoclonal antibodies directed against the immunodominant region of Tg. The smallest peptide (40 kDa) bore thyroid hormones and was identified at the C-terminal end of the Tg molecule, which shows homologies with acetylcholinesterase. Similar peptides were obtained by performing metal-mediated oxidation of Tg via a Fenton reaction. It was concluded that the oxidative stress induced during hormone synthesis generates free radicals, which, in turn, cleave Tg into immunoreactive peptides.
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Beck-Peccoz, Paolo, and Luca Persani. "Variable biological activity of thyroid-stimulating hormone." European Journal of Endocrinology 131, no. 4 (October 1994): 331–40. http://dx.doi.org/10.1530/eje.0.1310331.
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Beck-Peccoz P, Persani L. Variable biological activity of thyroid-stimulating hormone. Eur J Endocrinol 1994;131:331–40. ISSN 0804–4643 Thyroid-stimulating hormone (TSH), like the other pituitary glycoprotein hormones, is produced and secreted as a mixture of isoforms, the majority of which represent differences in oligosaccharide structure and possess different bioactivity. When samples are quantified simultaneously by immunometric assay and bioassay, the ratio between bioactivity (B) and immunoreactivity (I) may serve as an index of the overall potency of TSH. Variations of the TSH B/I ratio have been documented in both physiological and pathological conditions associated with alteration of the two most important mechanisms controlling TSH synthesis and secretion, i.e. TRH release and the thyroid hormone feedback system. Major examples of this assumption are the low TSH bioactivity found in samples from patients lacking TRH and thus bearing a hypothalamic hypothyroidism, and the enhanced bioactivity that is invariably found in TSH from patients with thyroid hormone resistance. Moreover, variations of TSH bioactivity have been recorded in normal subjects during the nocturnal TSH surge, in normal fetuses during the last trimester of pregnancy, in patients with primary hypothyroidism and in patients with TSH-secreting pituitary adenoma and non-thyroidal illness. In conclusion, the secretion of TSH molecules with altered bioactivity plays an important pathogenetic role in various thyroid disorders, while in some particular physiological conditions the bioactivity of TSH may vary in order to adjust thyroid hormone secretion to temporary needs. Paolo Beck-Peccoz, Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS, Via F. Sforza 35, 1-20122 Milano, Italy
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Braverman, L. E. "Evaluation of thyroid status in patients with thyrotoxicosis." Clinical Chemistry 42, no. 1 (January 1, 1996): 174–78. http://dx.doi.org/10.1093/clinchem/42.1.174.
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Abstract The generic term thyrotoxicosis defines the clinical syndrome of hypermetabolism associated with excess amounts of circulating free thyroxine (T4) and (or) triiodothyronine (T3) concentrations, irrespective of the source of the excess hormones. The term hyperthyroidism is reserved for those patients with thyrotoxicosis caused by increased synthesis and secretion of thyroid hormones from the gland due either to thyroid stimulators in the blood or to autonomously functioning thyroid nodules and is almost always associated with an increased radioactive iodine uptake (RAIU) by the thyroid. Another major cause of thyrotoxicosis is increased release of thyroid hormone from the gland, not associated with increased synthesis, caused by inflammatory changes, and always associated with a low thyroid RAIU. The most common miscellaneous cause of thyrotoxicosis is the exogenous ingestion of excess thyroid hormone, associated with a low thyroid RAIU. The serum concentration of thyrotropin (TSH) is low in all causes of thyrotoxicosis, except for TSH-secreting pituitary tumors and selective pituitary resistance to thyroid hormones. Anti-thyroglobulin and anti-thyroid peroxidase antibodies are present in patients with autoimmune thyroid disease, and serum thyroglobulin is increased in all patients with thyrotoxicosis except those with thyrotoxicosis facticia. A decreased serum TSH and normal concentrations of serum free T4 and T3 define the syndrome of subclinical thyrotoxicosis.
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Chiamolera, Maria Izabel, and Fredric E. Wondisford. "Thyrotropin-Releasing Hormone and the Thyroid Hormone Feedback Mechanism." Endocrinology 150, no. 3 (January 29, 2009): 1091–96. http://dx.doi.org/10.1210/en.2008-1795.
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Thyroid hormone (TH) plays a critical role in development, growth, and cellular metabolism. TH production is controlled by a complex mechanism of positive and negative regulation. Hypothalamic TSH-releasing hormone (TRH) stimulates TSH secretion from the anterior pituitary. TSH then initiates TH synthesis and release from the thyroid gland. The synthesis of TRH and TSH subunit genes is inhibited at the transcriptional level by TH, which also inhibits posttranslational modification and release of TSH. Although opposing TRH and TH inputs regulate the hypothalamic-pituitary-thyroid axis, TH negative feedback at the pituitary was thought to be the primary regulator of serum TSH levels. However, study of transgenic animals showed an unexpected, dominant role for TRH in regulating the hypothalamic-pituitary-thyroid axis and an unanticipated involvement of the thyroid hormone receptor ligand-dependent activation function (AF-2) domain in TH negative regulation. These results are summarized in the review. The thyrotropin-releasing hormone neuron is well-positioned to integrate information about the environment as well as circulating TH levels and ultimately affect metabolism in response to these physiological changes.
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Thomas, Gerry. "A new route to thyrotoxicosis?" Human & Experimental Toxicology 14, no. 12 (December 1995): 994–95. http://dx.doi.org/10.1177/096032719501401210.
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Human thyrocytes were found to synthesise and secrete the selenoenzyme extracellular glutathione peroxidase (E-GPX), a process which was controlled by the Ca2+/phosphoinositol second messenger cas cade. The potential involvement of thyroidal E-GPX in the regulation of thyroid hormone synthesis and in the protection of the thyrocyte from peroxidative damage is discussed.
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Ząbczyńska, Marta, Kamila Kozłowska, and Ewa Pocheć. "Glycosylation in the Thyroid Gland: Vital Aspects of Glycoprotein Function in Thyrocyte Physiology and Thyroid Disorders." International Journal of Molecular Sciences 19, no. 9 (September 17, 2018): 2792. http://dx.doi.org/10.3390/ijms19092792.
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The key proteins responsible for hormone synthesis in the thyroid are glycosylated. Oligosaccharides strongly affect the function of glycosylated proteins. Both thyroid-stimulating hormone (TSH) secreted by the pituitary gland and TSH receptors on the surface of thyrocytes contain N-glycans, which are crucial to their proper activity. Thyroglobulin (Tg), the protein backbone for synthesis of thyroid hormones, is a heavily N-glycosylated protein, containing 20 putative N-glycosylated sites. N-oligosaccharides play a role in Tg transport into the follicular lumen, where thyroid hormones are produced, and into thyrocytes, where hyposialylated Tg is degraded. N-glycans of the cell membrane transporters sodium/iodide symporter and pendrin are necessary for iodide transport. Some changes in glycosylation result in abnormal activity of the thyroid and alteration of the metabolic clearance rate of hormones. Alteration of glycan structures is a pathological process related to the progression of chronic diseases such as thyroid cancers and autoimmunity. Thyroid carcinogenesis is accompanied by changes in sialylation and fucosylation, β1,6-branching of glycans, the content and structure of poly-LacNAc chains, as well as O-GlcNAcylation, while in thyroid autoimmunity the main processes affected are sialylation and fucosylation. The glycobiology of the thyroid gland is an intensively studied field of research, providing new data helpful in understanding the role of the sugar component in thyroid protein biology and disorders.
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Müller, Kathrin, Dagmar Führer, Jens Mittag, Nora Klöting, Matthias Blüher, Roy E. Weiss, Marie-Christine Many, Kurt Werner Schmid, and Knut Krohn. "TSH Compensates Thyroid-Specific IGF-I Receptor Knockout and Causes Papillary Thyroid Hyperplasia." Molecular Endocrinology 25, no. 11 (November 1, 2011): 1867–79. http://dx.doi.org/10.1210/me.2011-0065.
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Abstract Although TSH stimulates all aspects of thyroid physiology IGF-I signaling through a tyrosine kinase-containing transmembrane receptor exhibits a permissive impact on TSH action. To better understand the importance of the IGF-I receptor in the thyroid in vivo, we inactivated the Igf1r with a Tg promoter-driven Cre-lox system in mice. We studied male and female mice with thyroidal wild-type, Igf1r+/−, and Igf1r−/− genotypes. Targeted Igf1r inactivation did transiently reduce thyroid hormone levels and significantly increased TSH levels in both heterozygous and homozygous mice without affecting thyroid weight. Histological analysis of thyroid tissue with Igf1r inactivation revealed hyperplasia and heterogeneous follicle structure. From 4 months of age, we detected papillary thyroid architecture in heterozygous and homozygous mice. We also noted increased body weight of male mice with a homozygous thyroidal null mutation in the Igf1r locus, compared with wild-type mice, respectively. A decrease of mRNA and protein for thyroid peroxidase and increased mRNA and protein for IGF-II receptor but no significant mRNA changes for the insulin receptor, the TSH receptor, and the sodium-iodide-symporter in both Igf1r+/− and Igf1r−/− mice were detected. Our results suggest that the strong increase of TSH benefits papillary thyroid hyperplasia and completely compensates the loss of IGF-I receptor signaling at the level of thyroid hormones without significant increase in thyroid weight. This could indicate that the IGF-I receptor signaling is less essential for thyroid hormone synthesis but maintains homeostasis and normal thyroid morphogenesis.
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Walker, Peter. "Neonatal hyperthyroidism alters submandibular gland epidermal growth factor response to thyroxine in the adult mouse." Canadian Journal of Physiology and Pharmacology 63, no. 9 (September 1, 1985): 1151–54. http://dx.doi.org/10.1139/y85-188.
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Neonatal hyperthyroidism (NH) in the rat is associated with permanent reductions in serum thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) concentrations in the adult, changes suggestive of a hypothyroid state. In the adult NH rat, the thyrotroph appears to be more sensitive to the feedback effects of thyroid hormones. To determine whether thyroid hormone sensitive tissues retain their responsiveness to thyroid hormones, the long-term effects of NH on mouse submandibular gland (SMG) epidermal growth factor (EGF) content were examined. NH was induced in female mice by 20 daily subcultaneous injections of 0.4 μg of T4 per gram of body weight. Control female mice received daily injections of vehicle alone. At 21 days of age, NH and control mice were sacrificed and SMG EGF content was measured by specific radioimmunoassay. SMG EGF content and concentration in 21-day-old NH mice exceeded that of control mice by 2400- and 1500-fold, respectively (P < 0.001). SMG EGF content and concentration in adult (90-day-old) NH mice were slightly, but not significantly, lower than those of control mice. Mean SMG weight, however, was significantly decreased in adult NH mice (P < 0.01). Interestingly, SMG content and concentration of EGF in adult NH mice were lower than in 21-day-old NH mice. After 5 days T4 treatment (16 μg/d) of adult mice, SMG weight in NH mice increased significantly (P < 0.01) but was unchanged in control mice. SMG EGF content and concentration increased significantly in both adult NH and control mice (P < 0.01). However, the magnitude of the increase was markedly obtunded in adult NH mice. These observations indicate that thyroid hormones precociously and exponentially increase SMG EGF content and concentration in neonatal mice. The marked increases strongly suggest thyroid hormone mediated synthesis of EGF and acceleration of maturation of gene expression for EGF synthesis. In addition, NH appears to modify thyroid hormone regulation of gene expression for EGF synthesis in adult mice.
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Elbrecht, Alex, and Catherine B. Lazier. "Selective inhibitory effects of thyroid hormones on estrogen-induced protein synthesis in chick embryo liver." Canadian Journal of Biochemistry and Cell Biology 63, no. 12 (December 1, 1985): 1206–11. http://dx.doi.org/10.1139/o85-151.
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We have investigated the effect of thyroid hormones on estrogen-induced responses in embryonic chick liver. Administration of thyroid hormones inhibits estrogen induction of vitellogenin, as well as of apoprotein-II of very low density lipoprotein (VLDL apo-II). A proportionate decrease in the concentration of hepatic salt-soluble nuclear estrogen receptor is also observed. In contrast, estrogen stimulation of apoprotein-B (VLDL apo-B) synthesis is relatively resistant to inhibition. The inhibitory effects of the thyroid hormones could be due to increased metabolism and clearance of estradiol-17β in their presence. The relative resistance of estrogen-induced VLDL apo-B synthesis to thyroid hormone inhibition can be explained by its greater sensitivity to low doses of estradiol. In addition, experiments with the antithyroid agent thiourea suggest that, in vivo, estrogen-induced responses could be balanced by the selective inhibitory effects of thyroid hormones.
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Kacer, Martina, Dilys A. Whyte, Ivy Boydstun, and Thomas A. Wilson. "Congenital Nephrotic Syndrome and Persistent Hypothyroidism After Bilateral Nephrectomy." Journal of Pediatric Endocrinology and Metabolism 21, no. 6 (June 1, 2008): 597–602. http://dx.doi.org/10.1515/jpem-2008-210615.
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Abstract Congenital nephrotic syndrome is commonly associated with hypothyroidism. Thyroid hormone supplementation is recommended as standard of care. The hypothyroidism is postulated to occur secondary to chronic massive proteinuria with loss of thyroid binding globulin, thyroid hormone and iodine. Previous reports have indicated that thyroxin may be discontinued following bilateral nephrectomy. We report our experience with one child with congenital nephrotic syndrome, Finnish type, and hypothyroidism who had a high requirement for thyroxin (100-150 μg/d) from infancy to 4 years of age. Hypothyroidism persisted despite bilateral nephrectomy and later following renal transplantation. However, his thyroxin requirement is now substantially lower (62.5 μg/d) at age 14 years. No goiter was detected clinically and antithyroid antibodies were negative. Thyroid ultrasound and 1231 scan revealed a thyroid gland in the anatomically normal location. 1231 uptake was elevated, 18% at 6 hours and 51% at 24 hours (normal values: 3-16% at 6 hours and 8- 25% at 24 hours). Perchlorate was unavailable for a perchlorate washout study. We speculate that this patient may have an intrinsic problem with thyroid hormone synthesis. It is unclear whether this is related or coincidental to the Finnish nephrotic syndrome. We recommend following thyroid functions closely if thyroxin is discontinued following bilateral nephrectomies in Finnish type congenital nephrotic syndrome.
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Noh, Jaeduk, Noboru Hamada, Hifumi Saito, Midori Yoshimoto, Hiroyuki Iwasaki, Osamu Ozaki, Yasuyuki Okamoto, Kunihiko Ito, and Hirotoshi Morii. "Inhibition by immunoglobulin G of synthesis of thyroid hormone in thyroid cultures from hypothyroid patients with goitrous Hashimoto's thyroiditis." Acta Endocrinologica 123, no. 5 (November 1990): 511–18. http://dx.doi.org/10.1530/acta.0.1230511.
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Abstract. Recently, thyroid microsomal antigen was identified as thyroid peroxidase, and thyroid microsomal antibody was found to inhibit thyroid peroxidase activity in vitro. We investigated the possibility that anti-microsomal antibody inhibits the iodination of tyrosine, in vivo. Immunoglobulin G with or without anti-microsomal antibody from hypothyroid patients with goitrous Hashimoto's thyroiditis inhibited thyroid hormone synthesis in cultured slices of normal human thyroid tissue. IgGs with anti-microsomal antibody inhibited 125I thyroidal uptake and thyroid hormone synthesis stimulated by TSH more than normal IgG did. However, the same results were obtained with IgGs without anti-microsomal antibody. This effect did not involve anti-microsomal antibody, anti-thyroglobulin antibody, TSH-binding inhibitor immunoglobulin, thyroid stimulation-blocking immunoglobulin, or the cAMP level of the thyroid tissue. The ratio of organic I to inorganic I with stimulation by TSH in slices incubated with IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis or normal IgG was not significantly different, but was significantly higher in slices incubated with methylmercaptoimidazole. Therefore, IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis mainly suppressed 125I thyroidal uptake, rather than inhibiting thyroid peroxidase activity. In addition, this IgG was present in the serum of 11 of the 12 hypothyroid patients with Hashimoto's thyroiditis studied. This IgG may be involved in the mechanism that causes hypothyroidism in some patients with goitrous Hashimoto's disease.
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Dunn, John T. "Thyroglobulin, hormone synthesis and thyroid disease." European Journal of Endocrinology 132, no. 5 (May 1995): 603–4. http://dx.doi.org/10.1530/eje.0.1320603.
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Gillam, Mary P., and Peter Kopp. "Genetic defects in thyroid hormone synthesis." Current Opinion in Pediatrics 13, no. 4 (August 2001): 364–72. http://dx.doi.org/10.1097/00008480-200108000-00014.
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Ren, Bingtao, and Yan Zhu. "A New Perspective on Thyroid Hormones: Crosstalk with Reproductive Hormones in Females." International Journal of Molecular Sciences 23, no. 5 (February 28, 2022): 2708. http://dx.doi.org/10.3390/ijms23052708.
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Accumulating evidence has shown that thyroid hormones (THs) are vital for female reproductive system homeostasis. THs regulate the reproductive functions through thyroid hormone receptors (THRs)-mediated genomic- and integrin-receptor-associated nongenomic mechanisms, depending on TH ligand status and DNA level, as well as transcription and extra-nuclear signaling transduction activities. These processes involve the binding of THs to intracellular THRs and steroid hormone receptors or membrane receptors and the recruitment of hormone-response elements. In addition, THs and other reproductive hormones can activate common signaling pathways due to their structural similarity and shared DNA consensus sequences among thyroid, peptide, and protein hormones and their receptors, thus constituting a complex and reciprocal interaction network. Moreover, THs not only indirectly affect the synthesis, secretion, and action of reproductive hormones, but are also regulated by these hormones at the same time. This crosstalk may be one of the pivotal factors regulating female reproductive behavior and hormone-related diseases, including tumors. Elucidating the interaction mechanism among the aforementioned hormones will contribute to apprehending the etiology of female reproductive diseases, shedding new light on the treatment of gynecological disorders.
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Chung, Shinjae, Xiao-Hui Liao, Caterina Di Cosmo, Jacqueline Van Sande, Zhiwei Wang, Samuel Refetoff, and Olivier Civelli. "Disruption of the Melanin-Concentrating Hormone Receptor 1 (MCH1R) Affects Thyroid Function." Endocrinology 153, no. 12 (December 1, 2012): 6145–54. http://dx.doi.org/10.1210/en.2011-1435.
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Abstract Melanin-concentrating hormone (MCH) is a peptide produced in the hypothalamus and the zona incerta that acts on one receptor, MCH receptor 1 (MCH1R), in rodents. The MCH system has been implicated in the regulation of several centrally directed physiological responses, including the hypothalamus-pituitary-thyroid axis. Yet a possible direct effect of the MCH system on thyroid function has not been explored in detail. We now show that MCH1R mRNA is expressed in thyroid follicular cells and that mice lacking MCH1R [MCH1R-knockout (KO)] exhibit reduced circulating iodothyronine (T4, free T4, T3, and rT3) levels and high TRH and TSH when compared with wild-type (WT) mice. Because the TSH of MCH1R-KO mice displays a normal bioactivity, we hypothesize that their hypothyroidism may be caused by defective thyroid function. Yet expression levels of the genes important for thyroid hormones synthesis or secretion are not different between the MCH1R-KO and WT mice. However, the average thyroid follicle size of the MCH1R-KO mice is larger than that of WT mice and contained more free and total T4 and T3 than the WT glands, suggesting that they are sequestered in the glands. Indeed, when challenged with TSH, the thyroids of MCH1R-KO mice secrete lower amounts of T4. Similarly, secretion of iodothyronines in the plasma upon 125I administration is significantly reduced in MCH1R-KO mice. Therefore, the absence of MCH1R affects thyroid function by disrupting thyroid hormone secretion. To our knowledge, this study is the first to link the activity of the MCH system to the thyroid function.
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Ma, Yaluan, Patricia Freitag, Jie Zhou, Bernhard Brüne, Stilla Frede, and Joachim Fandrey. "Thyroid hormone induces erythropoietin gene expression through augmented accumulation of hypoxia-inducible factor-1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 3 (September 2004): R600—R607. http://dx.doi.org/10.1152/ajpregu.00115.2004.
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Oxygen is of vital importance for the metabolism and function of all cells in the human body. Hypoxia, the reduction of oxygen supply, results in adaptationally appropriate alterations in gene expression through the activation of hypoxia-inducible factor 1 (HIF-1) to overcome any shortage of oxygen. Thyroid hormones are required for normal function of nearly all tissues, with major effects on oxygen consumption and metabolic rate. Thyroid hormones have been found to augment the oxygen capacity of the blood by increasing the production of erythropoietin (EPO) and to improve perfusion by vasodilation through the augmented expression of adrenomedullin (ADM). Because the hypoxic expression of both genes depends on HIF-1, we studied the influence of thyroid hormone on HIF-1 activation in the human hepatoma cell line HepG2 under normoxic and hypoxic conditions. We found that thyroid hormones increased HIF-1α protein accumulation by increasing HIF-1α protein synthesis rather than attenuating its proteasomal degradation. HIF-1α expression directly correlated with augmented HIF-1 DNA binding and transcriptional activity of luciferase reporter plasmids, whereas HIF-1β levels remained unaffected. Knocking down HIF-1α by short interfering RNA (siRNA) clearly demonstrated that thyroid hormone-induced target gene expression required the presence of HIF-1. Although an increased association of the two known coactivators of HIF-1, p300 and SRC-1, was found, thyroid hormone did not affect the activity of the isolated COOH-terminal transactivating domain of HIF-1α. Increased synthesis of HIF-1α may contribute to the adaptive response of increased oxygen demand under hyperthyroid conditions.
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Akhter, S., ZU Nahar, S. Parvin, A. Alam, S. Sharmin, and MI Arslan. "Thyroid Status in Patients with Low Serum Ferritin Level." Bangladesh Journal of Medical Biochemistry 5, no. 1 (January 20, 2013): 5–11. http://dx.doi.org/10.3329/bjmb.v5i1.13424.
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Iron deficiency is the most important but preventable nutritional problem in Bangladesh. Thyroid peroxidase, an iron containing enzyme, is essential for initial two steps of thyroid hormone synthesis which is a component of tissue iron. Tissue iron diminishes early in the course of iron deficiency. So thyroid hormone level may be altered in iron deficient patients. This case-control study was carried out in the Department of Biochemistry, Bangabandhu Sheikh Mujib Medical University (BSMMU) from July 2006 to June 2007. This study was done to find out the changes of thyroid hormonal activity in iron deficiency.In this study 72 subjects were selected from the out-patient department of the hospital. Patients with low serum ferritin level <12 mgm/L were selected as cases (n=36) and healthy persons with normal serum ferritin level were taken as controls. Serum ferritin, thyroid stimulating hormone (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) were measured in all study subjects. Values were expressed as mean ± SD. Unpaired 't' test and Pearson's correlation test were performed to see the level of significance and p value <0.05 was taken as significant. Serum ferritin level in cases and controls were 6.78±4.05 mgm/L and 79.04±28.08 mgm/L respectively which showed significant difference (P<0.0001).Serum TSH concentration in cases and controls were 3.32±1.54 mIU/L and 1.89±0.86 mIU/L respectively. Serum FT4 concentration in cases and controls were 11.66±1.77 pmol/L and 13/10±1.36 pmol/L respectively and that of FT3 were 3.00±0.68 and 3.31±0.61 pmol/L respectively. All showed significant difference between groups.Serum ferritin and Serum TSH showed significant negative correlation in controls whereas in cases they showed negative correlation which was not statistically significant.Both serum FT4 and FT3 revealed positive correlation with serum ferritin but that too was not significant statistically.Though the study failed to show any significant positive correlation between serum ferritin and thyroid hormones, lower level of thyroid status in iron deficient patients suggest that it could be a reflection of disturbed activities of iron dependent enzymes such as thyroid peroxidase that impairs thyroid hormone synthesis. However, a large scale study is recommeded to establish the fact.This study showed that there was significant difference in thyroid hormonal status between iron deficient patients and normal healthy persons. Therefore it can be concluded that iron deficiency may impair normal thyroid hormone status. DOI: http://dx.doi.org/10.3329/bjmb.v5i1.13424 Bangladesh J Med Biochem 2012; 5(1): 5-11
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McKinnon, Brett, Huika Li, Kerry Richard, and Robin Mortimer. "Synthesis of Thyroid Hormone Binding Proteins Transthyretin and Albumin by Human Trophoblast." Journal of Clinical Endocrinology & Metabolism 90, no. 12 (December 1, 2005): 6714–20. http://dx.doi.org/10.1210/jc.2005-0696.
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Context: Mechanisms regulating materno-fetal transfer of thyroid hormone are not well understood. Modulation of trophoblast type 3 iodothyronine deiodinase (D3) may play an important role. Objective: The objective of this study was to investigate trophoblast thyroid hormone binding proteins that may modulate interactions between D3 and T4. Design: Placentas were obtained by informed consent from women delivering normal infants by repeat cesarean section at 38–40 wk gestation. T4 and T3 binding was examined in human placenta. Serum thyroid hormone binding proteins were identified by Western blotting, and their mRNA was examined by RT-PCR. Presence of these proteins in trophoblast was determined by immunocytochemistry and immunofluorescence. Cytosol was progressively purified to reveal additional thyroid hormone binding proteins that were identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry. Effects of mefenamic acid on placental deiodination were examined by HPLC. Results: We detected high-affinity T4 and T3 binding in human placental cytosol. All three major serum-binding proteins, T4 binding globulin (TBG), transthyretin (TTR), and albumin, were present in cytosol. TTR mRNA and albumin mRNA were detected in human placenta, and TTR and albumin were identified histochemically in syncytiotrophoblasts. Neither TBG mRNA nor TBG was detected, suggesting that plasma TBG had contaminated the cytosol preparation. Low-affinity thyroid hormone binding proteins α-1-antitrypsin and α-1-acid glycoprotein were also identified. Addition of mefenamic acid, a potent inhibitor of thyroid hormone binding, to placental cytosol significantly enhanced deiodination of T4 by D3. Conclusions: Placenta produces a series of thyroid hormone binding proteins that may modify thyroid hormone deiodination and materno-fetal thyroid hormone transport.
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Rosen, Meghan D., and Martin L. Privalsky. "Thyroid Hormone Receptor Mutations in Cancer and Resistance to Thyroid Hormone: Perspective and Prognosis." Journal of Thyroid Research 2011 (2011): 1–20. http://dx.doi.org/10.4061/2011/361304.
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Thyroid hormone, operating through its receptors, plays crucial roles in the control of normal human physiology and development; deviations from the norm can give rise to disease. Clinical endocrinologists often must confront and correct the consequences of inappropriately high or low thyroid hormone synthesis. Although more rare, disruptions in thyroid hormone endocrinology due to aberrations in the receptor also have severe medical consequences. This review will focus on the afflictions that are caused by, or are closely associated with, mutated thyroid hormone receptors. These include Resistance to Thyroid Hormone Syndrome, erythroleukemia, hepatocellular carcinoma, renal clear cell carcinoma, and thyroid cancer. We will describe current views on the molecular bases of these diseases, and what distinguishes the neoplastic from the non-neoplastic. We will also touch on studies that implicate alterations in receptor expression, and thyroid hormone levels, in certain oncogenic processes.
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Luci, Bettzieche, and Eder. "Research Paper Effects of 13-HPODE on Expression of Genes Involved in Thyroid Hormone Synthesis, Iodide Uptake and Formation of Hydrogen Peroxide in Porcine Thyrocytes." International Journal for Vitamin and Nutrition Research 76, no. 6 (November 1, 2006): 398–406. http://dx.doi.org/10.1024/0300-9831.76.6.398.
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It has been shown that dietary oxidized fats influence thyroid function in rats and pigs. Mechanisms underlying this phenomenon are unknown. This study was performed to investigate whether 13-hydroperoxy-9,11-octadecadienic acid (13-HPODE), a primary oxidation product of linoleic acid, affects expression of genes involved in thyroid hormone synthesis and formation of hydrogen peroxide in primary porcine thyrocytes. Thyrocytes were treated with 13-HPODE in concentrations between 20 and 100 μM. Cells treated with vehicle alone ("control cells") or with equivalent concentrations of linoleic acid were considered as controls. Treatment of cells with 13-HPODE did not affect cell viability but increased the activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase (p < 0.05) compared to control cells or cells treated with linoleic acid. Relative mRNA concentrations of genes involved in thyroid hormone synthesis like sodium iodide symporter, thyrotropin receptor, and thyroid peroxidase, as well as iodide uptake, did not differ between cells treated with 13-HPODE and control cells or cells treated with linoleic acid. Treatment of cells with 13-HPODE, however, reduced the relative mRNA concentrations of dual oxidase-2 and the formation of hydrogen peroxide compared to control cells or cells treated with linoleic acid (p < 0.05). Because the production of hydrogen peroxide is rate-limiting for the synthesis of thyroid hormones, it is suggested that 13-HPODE could have an impact on the formation of thyroid hormones in the thyroid gland.
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Ballock, R. Tracy, Xiaolan Zhou, Lynn M. Mink, Daniel H. C. Chen, Barry C. Mita, and Matthew C. Stewart. "Expression of Cyclin-Dependent Kinase Inhibitors in Epiphyseal Chondrocytes Induced to Terminally Differentiate with Thyroid Hormone." Endocrinology 141, no. 12 (December 1, 2000): 4552–57. http://dx.doi.org/10.1210/endo.141.12.7839.
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Abstract A growing body of evidence suggests that systemic hormones and peptide growth factors may exert their effects on cell growth and differentiation in part through regulation of the cell division cycle. We hypothesized that thyroid hormone regulates terminal differentiation of growth plate chondrocytes in part through controlling cell cycle progression at the G1/S restriction point. Our results support this hypothesis by demonstrating that treatment of epiphyseal chondrocytes with thyroid hormone under chemically defined conditions results in the arrest of DNA synthesis and the onset of terminal differentiation, indicating that thyroid hormone is one factor capable of regulating the transition between cell growth and differentiation in these cells. This terminal differentiation process is associated with induction of the cyclin/cyclin-dependent kinase inhibitors p21cip-1, waf-1 and p27kip1, suggesting that thyroid hormone may regulate terminal differentiation in part by arresting cell cycle progression through induction of cyclin-dependent kinase inhibitors.
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Senou, Maximin, Maria José Costa, Claude Massart, Matthieu Thimmesch, Céline Khalifa, Sylvie Poncin, Marie Boucquey, et al. "Role of caveolin-1 in thyroid phenotype, cell homeostasis, and hormone synthesis: in vivo study of caveolin-1 knockout mice." American Journal of Physiology-Endocrinology and Metabolism 297, no. 2 (August 2009): E438—E451. http://dx.doi.org/10.1152/ajpendo.90784.2008.
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In human thyroid, caveolin-1 is localized at the apex of thyrocytes, but its role there remains unknown. Using immunohistochemistry, 127I imaging, transmission electron microscopy, immunogold electron microscopy, and quantification of H2O2, we found that in caveolin-1 knockout mice thyroid cell homeostasis was disrupted, with evidence of oxidative stress, cell damage, and apoptosis. An even more striking phenotype was the absence of thyroglobulin and iodine in one-half of the follicular lumina and their presence in the cytosol, suggesting that the iodide organification and binding to thyroglobulin were intracellular rather than at the apical membrane/extracellular colloid interface. The latter abnormality may be secondary to the observed mislocalization of the thyroid hormone synthesis machinery (dual oxidases, thyroperoxidase) in the cytosol. Nevertheless, the overall uptake of radioiodide, its organification, and secretion as thyroid hormones were comparable to those of wild-type mice, suggesting adequate compensation by the normal TSH retrocontrol. Accordingly, the levels of free thyroxine and TSH were normal. Only the levels of free triiodothyronine showed a slight decrease in caveolin-1 knockout mice. However, when TSH levels were increased through low-iodine chow and sodium perchlorate, the induced goiter was more prominent in caveolin-1 knockout mice. We conclude that caveolin-1 plays a role in proper thyroid hormone synthesis as well as in cell number homeostasis. Our study demonstrates for the first time a physiological function of caveolin-1 in the thyroid gland. Because the expression and subcellular localization of caveolin-1 were similar between normal human and murine thyroids, our findings in caveolin-1 knockout mice may have direct relevance to the human counterpart.
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Howie, A. F., S. W. Walker, B. Åkesson, J. R. Arthur, and G. J. Beckett. "Thyroidal extracellular glutathione peroxidase: a potential regulator of thyroid-hormone synthesis." Biochemical Journal 308, no. 3 (June 15, 1995): 713–17. http://dx.doi.org/10.1042/bj3080713.
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Human thyrocytes were found to synthesize and secrete the selenoenzyme extracellular glutathione peroxidase (E-GPX), a process which was controlled by the Ca2+/phosphoinositol second-messenger cascade. The potential involvement of thyroidal E-GPX in the regulation of thyroid-hormone synthesis and in the protection of the thyrocyte from peroxidative damage is discussed.
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Lin, Hung-Yun, Paul M. Yen, Faith B. Davis, and Paul J. Davis. "Protein synthesis-dependent potentiation by thyroxine of antiviral activity of interferon-γ." American Journal of Physiology-Cell Physiology 273, no. 4 (October 1, 1997): C1225—C1232. http://dx.doi.org/10.1152/ajpcell.1997.273.4.c1225.
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We have studied the prenuclear signal transduction pathway by which thyroid hormone potentiates the antiviral activity of human interferon-γ (IFN-γ) in HeLa cells, which are deficient in thyroid hormone receptor (TR). The action of thyroid hormone was compared with that of milrinone, which has structural homologies with thyroid hormone.l-Thyroxine (T4), 3,5,3′-l-triiodothyronine (T3), and milrinone enhanced the antiviral activity of IFN-γ up to 100-fold, a potentiation blocked by cycloheximide. The 5′-deiodinase inhibitor 6- n-propyl-2-thiouracil did not block the T4 effect. 3,3′,5,5′-Tetraiodothyroacetic acid prevented the effect of T4 but not of milrinone. The effects of T4 and milrinone were blocked by inhibitors of protein kinases C (PKC) and A (PKA) and restored by PKC and PKA agonists; only the effect of T4 was blocked by genistein, a tyrosine kinase inhibitor. In separate models, milrinone was shown not to interact with nuclear TR-β. T4 potentiation of the antiviral activity of IFN-γ requires PKC, PKA, and tyrosine kinase activities but not traditional TR.
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Meischl, Christof, Henk P. Buermans, Thierry Hazes, Marian J. Zuidwijk, René J. P. Musters, Christa Boer, Arthur van Lingen, et al. "H9c2 cardiomyoblasts produce thyroid hormone." American Journal of Physiology-Cell Physiology 294, no. 5 (May 2008): C1227—C1233. http://dx.doi.org/10.1152/ajpcell.00328.2007.
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Thyroid hormone acts on a wide range of tissues. In the cardiovascular system, thyroid hormone is an important regulator of cardiac function and cardiovascular hemodynamics. Although some early reports in the literature suggested an unknown extrathyroidal source of thyroid hormone, it is currently thought to be produced exclusively in the thyroid gland, a highly specialized organ with the sole function of generating, storing, and secreting thyroid hormone. Whereas most of the proteins necessary for thyroid hormone synthesis are thought to be expressed exclusively in the thyroid gland, we now have found evidence that all of these proteins, i.e., thyroglobulin, DUOX1, DUOX2, the sodium-iodide symporter, pendrin, thyroid peroxidase, and thyroid-stimulating hormone receptor, are also expressed in cardiomyocytes. Furthermore, we found thyroglobulin to be transiently upregulated in an in vitro model of ischemia. When performing these experiments in the presence of 125I, we found that 125I was integrated into thyroglobulin and that under ischemia-like conditions the radioactive signal in thyroglobulin was reduced. Concomitantly we observed an increase of intracellularly produced, 125I-labeled thyroid hormone. In conclusion, our findings demonstrate for the first time that cardiomyocytes produce thyroid hormone in a manner adapted to the cell's environment.
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Radman, Monique, and Michael Portman. "Thyroid Hormone in the Pediatric Intensive Care Unit." Journal of Pediatric Intensive Care 05, no. 04 (April 28, 2016): 154–61. http://dx.doi.org/10.1055/s-0036-1583280.
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AbstractThyroid hormones are key factors necessary for normal growth and development in children. They have tight control of metabolic rate and, as a result, frequently become altered in their synthesis and/or release during times of stress or critical illness. Disturbances in thyroid hormone homeostasis have been well described in several pathologic states, including sepsis/septic shock, renal failure, trauma, severe malnutrition, and following cardiopulmonary bypass. Specifically, a decrease in serum triiodothyronine (T3) and a concomitant increase in reverse triiodothyronine (rT3) levels are the most common changes observed. It is further noteworthy that serum thyroxine (T4), rT3, and T3 levels change in relation to severity of nonthyroidal illness. Many past investigators have speculated that these alterations are a teleological adaptation to severe illness and the increased metabolic demands that critical illness bears. However, this paradigm has been challenged through multiple avenues and has lost support over the past few years. Instead the “inflammatory hypothesis” has emerged implicating a cytokine surge as the mediator of thyroid hormone disruption. Overall, the demonstrated association between low thyroid hormone levels and poor clinical outcomes, the beneficial effects of thyroid hormone supplementation in multiple critically ill subpopulations, and the well-established safety profile of T3 therapy make thyroid hormone supplementation in the pediatric ICU worth consideration.
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Yaglova, N. V., and T. T. Berezov. "Regulation of thyroid and pituitary function by bacterial lipopolysaccharide." Biomeditsinskaya Khimiya 56, no. 2 (2010): 179–86. http://dx.doi.org/10.18097/pbmc20105602179.
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Activation of toll-like receptors-4 by bacterial lipopolysaccharide downregulates pituitary and thyroid function. Besides decrease of thyroid-stimulating hormone secretion lipopolysaccharide affects secretion in follicular thyroid cells directly. The endotoxin partialy activates and inhibits different phases of follicular thyrocytes' secretion. Lipopolysaccharide enhances thyroglobulin synthesis and exocytosis into follicular lumen and supresses its resorbtion.It results in sharp drop of blood thyroxine concentration without decrease of deiodinases-mediated thiroxine to triiodothyronine conversion. Stimulation of the lipopolysaccharide-pretreated thyroid gland with thyroid-stimulating hormone increases resorbtion of thyroglobulin and thyroid hormone production. Combined stimulation of the thyroid gland increases protein bound thyroxine and triiodothyronine serum concentration unlike only TSH stimulation resulting in increase of free thyroid hormone levels. It also prooves that binding capacity of thyroid hormone serum transport proteins during nonthyroidal illness syndrome remains normal.
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Kirsten, Denise. "The Thyroid Gland: Physiology and Pathophysiology." Neonatal Network 19, no. 8 (December 2000): 11–26. http://dx.doi.org/10.1891/0730-0832.19.8.11.
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The thyroid gland contains many follicular cells that store the thyroid hormones within the thyroglobulin molecule until they are needed by the body. The thyroid hormones, often referred to as the major metabolic hormones, affect virtually every cell in the body. Synthesis and secretion of the thyroid hormones depend on the presence of iodine and tyrosine as well as maturation of the hypothalamic-pituitary-thyroid system. Interruption of this development, as occurs with premature delivery, results in inadequate production of thyroid-stimulating hormone and thyroxine, leading to a variety of physiologic conditions. Pathologic conditions occur in the presence of insufficient thyroid production or a defect in the thyroid gland. Laboratory tests are important in diagnosing conditions of the thyroid gland. A thorough history in combination with clinical manifestations and radiologic findings are also useful in diagnosing specific thyroid conditions. Nurses play an important role in identifying and managing thyroid disorders and in providing supportive care to infants and their families.
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Golstein, J., B. Corvilain, F. Lamy, D. Paquer, and J. E. Dumont. "Effects of a selenium deficient diet on thyroid function of normal and perchlorate treated rats." Acta Endocrinologica 118, no. 4 (August 1988): 495–502. http://dx.doi.org/10.1530/acta.0.1180495.
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Abstract. Pregnant rats were submitted to a selenium-deficient diet immediately after mating; it was continued for 4 weeks after delivery. The pups were sacrificed at 3 and 4 weeks of age. Perchlorate, an antithyroid agent inhibiting iodide trapping in the thyroid, was administered via the drinking water to half of the rats. Rats submitted to a normal laboratory diet and to the experimental diet supplemented with selenium were used as controls. The effects of selenium deficiency were an increase in the number of growth abnormalities, growth retardation, and decreased seleno-dependent glutathione peroxidase (GSH-Px) activity in plasma and in various organs. These effects were relieved by selenium supplementation in the diet. Perchlorate treatment induced the classic picture of primary hypothyroidism. Selenium deficiency increased thyroid hormone levels in perchlorate-treated rats and in controls drinking tap water. In the latter group, it also decreased TSH plasma concentration and thyroid weight. These effects were partially reversed by Se supplementation. In vitro experiments, performed on adult rats, revealed increased radioiodide uptake and organification in glands from the rats submitted to the selenium-free diet. Plasma T3 half-life was similar in control and Se-deficient rats. These data suggest a higher efficiency of thyroid hormone synthesis in the thyroids of selenium-deficient rats, despite a lower thyroid stimulation as evaluated by serum TSH. They are compatible with the hypothesis that decreased selenium supply, leading to a decreased GSH-Px in the thyroid, increases hydrogen peroxide steady state level and thus thyroid peroxidase activity and thyroid hormone synthesis.
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Derkach, K. V., V. M. Bondareva, and A. O. Shpakov. "Influence of intranasally administered insulin on metabolic and hormonal parameters in adult male rats, impaired due to three-day fasting in the early postnatal period." Biomeditsinskaya Khimiya 68, no. 4 (2022): 263–71. http://dx.doi.org/10.18097/pbmc20226804263.
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Temporary cessation or restriction of breastfeeding can lead to metabolic disorders in adulthood. However, data on the effect of fasting in the early postnatal period on the functions of the endocrine system in adulthood are rare and contradictory. Approaches for the correction of metabolic and hormonal disorders caused by premature cessation of breastfeeding have not been developed yet. The aim of the work was to study the metabolic and hormonal parameters and changes in the hormonal status of the gonadal and thyroid systems in 10-month-old male rats with interruption of breastfeeding on days P19-P21, as well as to evaluate the restorative effect on them of four weeks of treatment with intranasal insulin (II) administered in the postnatal period (P28-P55) or in adulthood (P183-P210). Lactation interruption has been induced by treatment of lactating females with bromocriptine (10 mg/day/rat, P19-P21). Male rats with temporary cessation of breastfeeding developed characteristic signs of the metabolic syndrome (obesity, dyslipidemia, impaired glucose tolerance, hyperleptinemia), decreased levels of testosterone and thyroid hormones (fT4, tT3) and weakened the synthesis of testosterone and thyroxine, stimulated respectively by GnRH and thyroliberin. This was due to a decrease in the sensitivity of the testes to luteinizing hormone (LH) and the thyroid gland to thyroid-stimulating hormone (TSH). Treatment with II in early ontogenesis reduced body weight and fat, improved lipid profile, sensitivity to insulin, leptin, LH and TSH, restored the levels of testosterone and thyroid hormones and their stimulation by releasing factors. Treatment with II in adulthood normalized the levels of testosterone, thyroid hormones, their stimulation by releasing factors, but had a little effect on metabolic and hormonal parameters. The obtained data point to a wide range of metabolic and hormonal disorders in adult male rats with the “neonatal” model of metabolic syndrome and to the effectiveness of various strategies for their correction using long-term II treatment.
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Szkudlinski, Mariusz W., Valerie Fremont, Catherine Ronin, and Bruce D. Weintraub. "Thyroid-Stimulating Hormone and Thyroid-Stimulating Hormone Receptor Structure-Function Relationships." Physiological Reviews 82, no. 2 (April 1, 2002): 473–502. http://dx.doi.org/10.1152/physrev.00031.2001.
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This review focuses on recent advances in the structure-function relationships of thyroid-stimulating hormone (TSH) and its receptor. TSH is a member of the glycoprotein hormone family constituting a subset of the cystine-knot growth factor superfamily. TSH is produced by the pituitary thyrotrophs and released to the circulation in a pulsatile manner. It stimulates thyroid functions using specific membrane TSH receptor (TSHR) that belongs to the superfamily of G protein-coupled receptors (GPCRs). New insights into the structure-function relationships of TSH permitted better understanding of the role of specific protein and carbohydrate domains in the synthesis, bioactivity, and clearance of this hormone. Recent progress in studies on TSHR as well as studies on the other GPCRs provided new clues regarding the molecular mechanisms of receptor activation. Such advances are a result of extensive site-directed mutagenesis, peptide and antibody approaches, detailed sequence analyses, and molecular modeling as well as studies on naturally occurring gain- and loss-of-function mutations. This review integrates expanding information on TSH and TSHR structure-function relationships and summarizes current concepts on ligand-dependent and -independent TSHR activation. Special emphasis has been placed on TSH domains involved in receptor recognition, constitutive activity of TSHR, new insights into the evolution of TSH bioactivity, and the development of high-affinity TSH analogs. Such structural, physiological, pathophysiological, evolutionary, and therapeutic implications of TSH-TSHR structure-function studies are frequently discussed in relation to concomitant progress made in studies on gonadotropins and their receptors.
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Enríquez, José A., Patricio Fernández-Silva, Nuria Garrido-Pérez, Manuel J. López-Pérez, Acisclo Pérez-Martos, and Julio Montoya. "Direct Regulation of Mitochondrial RNA Synthesis by Thyroid Hormone." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 657–70. http://dx.doi.org/10.1128/mcb.19.1.657.
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ABSTRACT We have analyzed the influence of in vivo treatment and in vitro addition of thyroid hormone on in organello mitochondrial DNA (mtDNA) transcription and, in parallel, on the in organello footprinting patterns at the mtDNA regions involved in the regulation of transcription. We found that thyroid hormone modulates mitochondrial RNA levels and the mRNA/rRNA ratio by influencing the transcriptional rate. In addition, we found conspicuous differences between the mtDNA dimethyl sulfate footprinting patterns of mitochondria derived from euthyroid and hypothyroid rats at the transcription initiation sites but not at the mitochondrial transcription termination factor (mTERF) binding region. Furthermore, direct addition of thyroid hormone to the incubation medium of mitochondria isolated from hypothyroid rats restored the mRNA/rRNA ratio found in euthyroid rats as well as the mtDNA footprinting patterns at the transcription initiation area. Therefore, we conclude that the regulatory effect of thyroid hormone on mitochondrial transcription is partially exerted by a direct influence of the hormone on the mitochondrial transcription machinery. Particularly, the influence on the mRNA/rRNA ratio is achieved by selective modulation of the alternative H-strand transcription initiation sites and does not require the previous activation of nuclear genes. These results provide the first functional demonstration that regulatory signals, such as thyroid hormone, that modify the expression of nuclear genes can also act as primary signals for the transcriptional apparatus of mitochondria.
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Sui, Li, and M. E. Gilbert. "Pre- and Postnatal Propylthiouracil-Induced Hypothyroidism Impairs Synaptic Transmission and Plasticity in Area CA1 of the Neonatal Rat Hippocampus." Endocrinology 144, no. 9 (September 1, 2003): 4195–203. http://dx.doi.org/10.1210/en.2003-0395.
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Abstract Thyroid hormones are essential for neonatal brain development. It is well established that insufficiency of thyroid hormone during critical periods of development can impair cognitive functions. The mechanisms that underlie learning deficits in hypothyroid animals, however, are not well understood. As impairments in synaptic function are likely to contribute to cognitive deficits, the current study tested whether thyroid hormone insufficiency during development would alter quantitative characteristics of synaptic function in the hippocampus. Developing rats were exposed in utero and postnatally to 0, 3, or 10 ppm propylthiouracil (PTU), a thyroid hormone synthesis inhibitor, administered in the drinking water of dams from gestation d 6 until postnatal day (PN) 30. Excitatory postsynaptic potentials and population spikes were recorded from the stratum radiatum and the pyramidal cell layer, respectively, in area CA1 of hippocampal slices from offspring between PN21 and PN30. Baseline synaptic transmission was evaluated by comparing input-output relationships between groups. Paired-pulse facilitation, paired-pulse depression, long-term potentiation, and long-term depression were recorded to examine short- and long-term synaptic plasticity. PTU reduced thyroid hormones, reduced body weight gain, and delayed eye-opening in a dose-dependent manner. Excitatory synaptic transmission was increased by developmental exposure to PTU. Thyroid hormone insufficiency was also dose-dependently associated with a reduction paired-pulse facilitation and long-term potentiation of the excitatory postsynaptic potential and elimination of paired-pulse depression of the population spike. The results indicate that thyroid hormone insufficiency compromises the functional integrity of synaptic communication in area CA1 of developing rat hippocampus and suggest that these changes may contribute to learning deficits associated with developmental hypothyroidism.
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Roy, Gouriprasanna, Munirathinam Nethaji, and G. Mugesh. "Biomimetic Studies on Anti-Thyroid Drugs and Thyroid Hormone Synthesis." Journal of the American Chemical Society 126, no. 9 (March 2004): 2712–13. http://dx.doi.org/10.1021/ja039860g.
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Becks, G. P., D. K. Buckingham, J. F. Wang, I. D. Phillips, and D. J. Hill. "Regulation of thyroid hormone synthesis in cultured ovine thyroid follicles." Endocrinology 130, no. 5 (May 1992): 2789–94. http://dx.doi.org/10.1210/endo.130.5.1315258.
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Roy, Gouriprasanna, and G. Mugesh. "Bioinorganic Chemistry in Thyroid Gland: Effect of Antithyroid Drugs on Peroxidase-Catalyzed Oxidation and Iodination Reactions." Bioinorganic Chemistry and Applications 2006 (2006): 1–9. http://dx.doi.org/10.1155/bca/2006/23214.
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Propylthiouracil (PTU) and methimazole (MMI) are the most commonly used antithyroid drugs. The available data suggest that these drugs may block the thyroid hormone synthesis by inhibiting the thyroid peroxidase (TPO) or diverting oxidized iodides away from thyroglobulin. It is also known that PTU inhibits the selenocysteine-containing enzyme ID-1 by reacting with the selenenyl iodide intermediate (E-SeI). In view of the current interest in antithyroid drugs, we have recently carried out biomimetic studies to understand the mechanism by which the antithyroid drugs inhibit the thyroid hormone synthesis and found that the replacement of sulfur with selenium in MMI leads to an interesting compound that may reversibly block the thyroid hormone synthesis. Our recent results on the inhibition of lactoperoxidase (LPO)-catalyzed oxidation and iodination reactions by antithyroid drugs are described.
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Franklyn, J. A., T. Lynam, K. Docherty, D. B. Ramsden, and M. C. Sheppard. "Effect of hypothyroidism on pituitary cytoplasmic concentrations of messenger RNA encoding thyrotrophin β and α subunits, prolactin and growth hormone." Journal of Endocrinology 108, no. 1 (January 1986): 43–47. http://dx.doi.org/10.1677/joe.0.1080043.
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ABSTRACT Thyroid hormones may directly regulate gene expression in the anterior pituitary. In order to examine this possibility we have studied the effect of hypothyroidism in the rat on pituitary cytoplasmic concentrations of messenger RNA (mRNA) encoding thyrotrophin (TSH) β and α subunits, prolactin and GH. We demonstrated a marked increase in TSH β and α subunit mRNA, accompanied by a decrease in GH mRNA, in the hypothyroid state, changes largely reversed by thyroid hormone replacement. We have thus shown a direct influence of thyroid status on the pretranslational events occurring in pituitary hormone synthesis. The simultaneous rise in cytoplasmic TSH β and α mRNA levels and fall in GH mRNA in hypothyroidism suggests that thyroid status exerts a differential effect on the expression of these genes. J. Endocr. (1986) 108, 43–47
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Pitt-Rivers, Rosalind. "SOME FACTORS THAT AFFECT THYROID HORMONE SYNTHESIS." Annals of the New York Academy of Sciences 86, no. 2 (December 15, 2006): 362–72. http://dx.doi.org/10.1111/j.1749-6632.1960.tb42817.x.
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