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Introduction Increased serum levels of proinflammatory cytokines have been associated with nonthyroidal illness (NTI; Boelen et al. 1993 ), which is a state of altered thyroid hormone regulation and metabolism during illness
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and exert its full biologic activity. This activation, as well a s the inactivation of thyroid hormones, occurs not in the thyroid, but in the periphery through the action of iodothyronine deiodinases ( Eales & Brown 1993 , Mol et al. 1997 , 1998
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Introduction The heart is a major target organ for thyroid hormone (tri-iodothyronine, T 3 ) action. Thyroid hormone exerts its biological effects largely by influencing thyroid hormone-regulated gene expression via interactions with the high
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal
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( Castro et al. 2006 ). At variance with PTC, a mouse model for FTC was lacking until Kaneshige et al. (2000) described a mutant mouse with a mutation ( PV ) targeted to the thyroid hormone receptor β (THRB) locus. In a heterozygous condition
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paradox. How might a pituitary target site be involved in remodelling of hypothalamic neuroendocrine circuits – the hallmark of the seasonal response? The answer to this lies in the remarkable discovery of thyroid hormones (THs) as key seasonal switches
School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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Introduction Thyroid hormone controls gene expression by interacting with nuclear receptors (TRs), which are hormone-inducible transcriptional factors ( Lazar 1993 ). Two genes encode TRs, TRα and TRβ ( Freedman 1992 ). At least two
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Department of Endocrinology and Metabolism, Hypothalamic Integration Mechanisms, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
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). Spontaneous diminished food intake is known to be a part of a variety of illnesses, but has received only little attention as a potential mediator of the illness-induced changes in thyroid hormone (TH) homeostasis, despite its sometimes profound impact. For
Department of Animal Physiology, Departamento de Biología, Instituto de Zoología, Institute for Water and Wetland Research, Faculty of Science, Radboud University Nijmegen, Heyendaalseweg 135, 6525 AJ Nijmegen, The Netherlands
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Department of Animal Physiology, Departamento de Biología, Instituto de Zoología, Institute for Water and Wetland Research, Faculty of Science, Radboud University Nijmegen, Heyendaalseweg 135, 6525 AJ Nijmegen, The Netherlands
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Introduction Thyroid hormone regulates many important functions such as growth, salinity preference, oxygen consumption, nutrient metabolism, and metamorphosis in fish (reviewed by Eales (2006) and Blanton & Specker (2007) ). Under normal
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Introduction The hypothalamic–pituitary–thyroid (HPT) axis regulates metabolism and growth, reproduction, and brain development in vertebrates. Similarly, in fish, thyroid hormones (THs) have been demonstrated to regulate growth ( Huang et al
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Houston Methodist Research Institute, College of Arts and Sciences, Departments of Paediatrics, Children's Health Research Institute, Department of Molecular Physiology and Biophysics, The Third Affiliated Hospital of Guangzhou Medical University, Genomic Medicine Program, 6670 Bertner Ave, Houston, Texas 77030, USA
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Houston Methodist Research Institute, College of Arts and Sciences, Departments of Paediatrics, Children's Health Research Institute, Department of Molecular Physiology and Biophysics, The Third Affiliated Hospital of Guangzhou Medical University, Genomic Medicine Program, 6670 Bertner Ave, Houston, Texas 77030, USA
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these concerns, it is important to understand how to manage local production of FGF21 in desired target tissues and the consequences of changes in FGF21 concentrations. Thyroid hormones (THs) act as master regulators of metabolism and there is evidence