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Laboratório de Fisiologia Endócrina Doris Rosenthal, Laboratório de Biologia do Exercício, Instituto de Biofísica Carlos Chagas Filho and Instituto de Pesquisa Translacional em Saúde e Ambiente na Região Amazônica (INPeTAM), CCS-Bloco G- Cidade Universitria, Ilha do Fundo, Rio de Janeiro 21949-900, Brazil
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these unequivocal effects on energy metabolism, 3,5-T2 might also affect the hypothalamus–pituitary–thyroid axis. Horst et al . (1995) have shown that 3,5-T2 treatment reduced serum thyroid-stimulating hormone (TSH) and thyroxine (T 4 ) levels as well
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Introduction Central congenital hypothyroidism (CCH) is a rare disorder in which inadequate thyroid hormone biosynthesis occurs due to defective stimulation of a normal thyroid gland by thyroid stimulating hormone (TSH). The underlying molecular
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the cytoplasm, CRY and PER proteins translocate into the nucleus and form inhibitory complexes feeding negatively back on their own transcription. A daily rhythmicity of circulating thyroid-stimulating hormone (TSH) peaking at daytime in rats is well
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β sub-units of thyroid-stimulating hormone (TSH). These cells lack receptors for the hypothalamic thyrotropin-releasing hormone (TRH) ( Bockmann et al . 1997 ), and do not respond to conventional hypothalamic outputs. In mammals, the MT1 receptor co
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in an open or closed conformation, respectively ( Astapova & Hollenberg 2013 ). Concentrations of thyroid hormones in the circulation are regulated via the negative feedback loop by the action of thyroid-stimulating hormone (TSH). Beside these
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Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK
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Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK
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) ( Perros & Krassas 2009 , Bahn 2010 , Naik et al . 2010 ). In GD, thyroid-stimulating antibodies (TSAbs) directed against the TSH receptor (TSHR) activate the thyroid gland, leading to excessive production of thyroid hormone and thyrotoxicosis ( Rees
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is common, affecting up to 2% of the population, and the majority of these individuals will have overactivation of the TSHR either by supraphysiological concentrations of TSH in hypothyroidism or from thyroid stimulating antibodies in Graves
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diabetes were excluded from this study. Besides, healthy controls had no family history of thyroid autoimmune disease or other autoimmune diseases. Clinical parameters, including thyrotropin (TSH), free T3 (FT3), free T4 (FT4), thyroperoxidase antibody
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stimulates thyroid epithelial cells like TSH and induces thyrotoxicosis and goiter ( Shimojo et al . 1996 ). We previously reported the expression of TSHR in fat cells, the level of which is almost comparable with that in the thyroid ( Endo et al . 1995
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ectoderm. The AL contains five distinct hormone-producing cell types: somatotrophs, thyrotrophs, lactotrophs, corticotrophs and gonadotrophs, which secrete growth hormone (GH), thyroid-stimulating hormone (TSH), prolactin (PRL), adrenocorticotropin (ACTH