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Alvaro Souto Padron, Ruy Andrade Louzada Neto, Thiago Urgal Pantaleão, Maria Carolina de Souza dos Santos, Renata Lopes Araujo, Bruno Moulin de Andrade, Monique da Silva Leandro, João Pedro Saar Werneck de Castro, Andrea Claudia Freitas Ferreira, and Denise Pires de Carvalho

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

Open access

Nadia Schoenmakers, Kyriaki S Alatzoglou, V Krishna Chatterjee, and Mehul T Dattani

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

Open access

J Fahrenkrug, B Georg, J Hannibal, and H L Jørgensen

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

Open access

Shona Wood and Andrew Loudon

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

Open access

Joachim M Weitzel, Torsten Viergutz, Dirk Albrecht, Rupert Bruckmaier, Marion Schmicke, Armin Tuchscherer, Franziska Koch, and Björn Kuhla

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

Open access

Shuang-Xia Zhao, Shanli Tsui, Anthony Cheung, Raymond S Douglas, Terry J Smith, and J Paul Banga

) ( 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

Open access

Lei Zhang, Carol Paddon, Mark D Lewis, Fiona Grennan-Jones, and Marian Ludgate

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

Open access

Qinglei Yin, Liyun Shen, Yicheng Qi, Dalong Song, Lei Ye, Ying Peng, Yanqiu Wang, Zhou Jin, Guang Ning, Weiqing Wang, Dongping Lin, and Shu Wang

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

Open access

Toyoshi Endo and Tetsuro Kobayashi

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

Open access

Scott Haston, Saba Manshaei, and Juan Pedro Martinez-Barbera

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