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Perry Barrett Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Elena Ivanova Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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E Scott Graham Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Alexander W Ross Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Dana Wilson Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Helene Plé Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Julian G Mercer Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Francis J Ebling Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Sandrine Schuhler Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Sandrine M Dupré Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Andrew Loudon Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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Peter J Morgan Molecular Endocrinology Group, Division of Obesity and Metabolic Health and Aberdeen Centre for Energy Regulation and Obesity (ACERO), Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
Faculty of Life Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK

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indication of which cells in the ependymal layer express CRBPI. GPR50 is an orphan G-protein-coupled receptor with approximately 45% homology with melatonin receptors, but does not bind melatonin ( Reppert et al. 1996 , Drew et al. 1998 ). This

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Edra London Section on Endocrinology and Genetics WEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA

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Michelle Bloyd Section on Endocrinology and Genetics WEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA

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Constantine A Stratakis Section on Endocrinology and Genetics WEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA

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), melanin-concentrating hormone (MCH), and gamma-aminobutyric acid (GABA) neurons ( Fig. 2 ). TRH, melanocortin 4 receptor (MC4R), and MC3R act via G s α, while the GABA receptor acts through Gi/Go. The TRH gene is regulated by overlapping thyroid response

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Julia N C Toews Department of Cellular & Physiological Sciences, The University of British Columbia, Vancouver, Canada

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Geoffrey L Hammond Department of Cellular & Physiological Sciences, The University of British Columbia, Vancouver, Canada

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Victor Viau Department of Cellular & Physiological Sciences, The University of British Columbia, Vancouver, Canada

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mineralocorticoid receptor (MR) or glucocorticoid receptor (GR) and regulate glucocorticoid-dependent target genes ( Reul et al. 2015 , Spiga & Lightman 2015 , de Kloet et al. 2019 ). Importantly, it is widely assumed that it is the ‘free’ corticosterone

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Arturo Hernandez Center for Molecular Medicine, Maine Medical Center Research Institute, Maine Medical Center, Scarborough, Maine, USA
Graduate School for Biomedical Science and Engineering, University of Maine, Orono, Maine, USA
Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts, USA

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M Elena Martinez Center for Molecular Medicine, Maine Medical Center Research Institute, Maine Medical Center, Scarborough, Maine, USA

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binding of the most active TH, 3,5,3′-triiodothyronine (T3), to its nuclear receptors. These receptors are DNA-binding transcription factors and are encoded by two different genes, Thra and Thrb ( Pascual & Aranda 2013 ). Upon receptor binding and

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María F Andreoli Laboratory of Experimental Neurodevelopment, Institute of Development and Paediatric Research (IDIP), La Plata Children’s Hospital and Scientific Research Commission, Province of Buenos Aires (CIC-PBA), La Plata, Buenos Aires, Argentina
Argentine Research Council (CONICET), La Plata, Buenos Aires, Argentina

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Jose Donato Jr Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Isin Cakir Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA

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Mario Perello Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology (IMBICE, Argentine Research Council (CONICET), National University of La Plata and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)), La Plata, Buenos Aires, Argentina

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the reversion of leptin-resistant states. General aspects of leptin and its receptor: molecular leptin signalling Leptin is a 167-residue peptide hormone mainly produced by adipocytes and acts in the central nervous system to primarily

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Eleonore Fröhlich
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Anja Witke
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Barbara Czarnocka
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Richard Wahl
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effects of protirelin (TRH) on cultured porcine thyrocytes. Journal of Endocrinological Investigation 15 345 –351. Wan Y , Wang L & Wu T 1994 The expression of retinoid X receptor genes is regulated by all-trans- and 9

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George Fink Florey Institute of Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Genetics Lane, Parkville, Victoria 3010, Australia

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three hypothalamic regulatory peptide neurohormones: thyrotrophin-releasing factor (now thyrotrophin-releasing hormone, TRH), LH- and follicle-stimulating hormone (FSH)-releasing factor (now gonadotrophin-releasing hormone, GnRH) and somatostatin

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Roman A Romanov Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Vienna, Austria

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Alán Alpár MTA-SE NAP Research Group of Experimental Neuroanatomy and Developmental Biology, Hungarian Academy of Sciences, Budapest, Hungary
Department of Anatomy, Semmelweis University, Budapest, Hungary

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Tomas Hökfelt Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden

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Tibor Harkany Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Vienna, Austria
Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden

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steroidogenesis in, and corticosteroid release from, the adrenal cortex ( Munck et al . 1984 , McEwen & Stellar 1993 ). Corticosteroid action is then executed through glucocorticoid receptors ( Gustafsson et al . 1987 ), encoded by the Nr3c1 gene ( McEwen

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Alejandra Abeledo-Machado Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina

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Pablo Anibal Pérez Centro de Microscopía Electrónica, Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina

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María Andrea Camilletti Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina

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Erika Yanil Faraoni Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina

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Florencia Picech Centro de Microscopía Electrónica, Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina

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Juan Pablo Petiti Centro de Microscopía Electrónica, Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina

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Silvina Gutiérrez Centro de Microscopía Electrónica, Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina

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Graciela Diaz-Torga Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina

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synthesize and secrete prolactin constitutively, several hypothalamic factors contribute to prolactin release, including serotonin, thyrotropin-releasing hormone (TRH), oxytocin, and VIP. Nonetheless, the primary stimulus of prolactin synthesis and release is

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Natasha N Chattergoon Center for Developmental Health, Oregon Health and Science University, Portland, Oregon, USA
Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA

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within mere hours, while muscles in the limb are stimulated to grow; both processes under the regulation of T3 ( Brown & Cai 2007 ). Mammals do not, of course, develop by metamorphosis as found in anurans. However, many of the thyroid receptors and their

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