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School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
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al . 1998 ) and decreased expression of cerebral thyroid hormone receptor (TR) expression ( Kilby et al . 2000 ) in growth-restricted human fetuses are postulated to contribute to this neurodevelopmental morbidity. Examination of growth
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Introduction Thyroid hormone (TH) has a profound influence on normal development, differentiation and metabolism. Genomic actions of THs are mainly mediated and regulated by thyroid hormone receptors (THRs) ( Cheng et al. 2010 , Cioffi et
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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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TSH regulation, strongly support the hypothesis that 3,5-T2 functions as an agonist of the β isoform of thyroid hormone receptor (TR) in vivo . Figure 4 Type 1 (D1) and type 2 (D2) iodothyronine deiodinase activities in control rats and rats treated
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
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Department of Diabetes, Endocrinology and Nutrition, Hospital de Girona ‘Dr Josep Trueta’, Institut D’investigació Biomèdica de Girona (IdIBGi) and University of Girona, Girona, Spain
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CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
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CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
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Department of Clinical Science, KG Jebsen Center for Diabetes Research, University of Bergen, Bergen, Norway
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CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
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CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
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Department of Diabetes, Endocrinology and Nutrition, Hospital de Girona ‘Dr Josep Trueta’, Institut D’investigació Biomèdica de Girona (IdIBGi) and University of Girona, Girona, Spain
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, Ghorbani et al . 1997 , Cao et al . 2011 ) and also thyroid hormone receptor (TR) agonism ( Lin et al . 2015 , Alvarez-Crespo et al . 2016 ). However, the role of central THs in the control of WAT browning remains unclear. The aim of this study was
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Diagramatic representation of the hypothalamic–pituitary–thyroid axis with positive regulation (black) predominantly mediated by thyrotropin-releasing hormone (TRH) and negative (grey) feedback influences, predominantly mediated by thyroid hormone receptor (TR