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T V Novoselova Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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R Larder University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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D Rimmington University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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C Lelliott Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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E H Wynn Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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R J Gorrigan Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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P H Tate Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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L Guasti Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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The Sanger Mouse Genetics Project Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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S O’Rahilly University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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A J L Clark Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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D W Logan Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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A P Coll University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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L F Chan Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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Introduction Melanocortin receptor accessory protein (MRAP) and its paralogue MRAP2 are a recently identified class of small, single-pass transmembrane domain accessory proteins ( Chan et al . 2009 , Novoselova et al . 2013 ). Both MRAP and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0057
Volume/Issue:
Volume 230: Issue 1
Open access
Nadia Schoenmakers University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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Kyriaki S Alatzoglou University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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V Krishna Chatterjee University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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Mehul T Dattani University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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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

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-15-0341
Volume/Issue:
Volume 227: Issue 3
Open access
Pauline Campos College of Engineering, Mathematics and Physical Sciences, University of Exeter, Exeter, UK

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Jamie J Walker College of Engineering, Mathematics and Physical Sciences, University of Exeter, Exeter, UK
EPSRC Centre for Predictive Modelling in Healthcare, University of Exeter, Exeter, UK
Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK

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Patrice Mollard IGF, University of Montpellier, CNRS, INSERM, Montpellier, France

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trigger large and rapid calcium (Ca 2+ ) influx through voltage-gated channels. AP firing can therefore be assessed by measuring changes in concentrations of intracellular Ca 2+ ( Yasuda et al. 2004 ). Similarly, activation of neurotransmitter receptors

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-20-0028
Volume/Issue:
Volume 246: Issue 2
Open access
J Fahrenkrug Department of Clinical Biochemistry, Bispebjerg and Frederiksberg Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

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B Georg Department of Clinical Biochemistry, Bispebjerg and Frederiksberg Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

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J Hannibal Department of Clinical Biochemistry, Bispebjerg and Frederiksberg Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

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H L Jørgensen Department of Clinical Biochemistry, Bispebjerg and Frederiksberg Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

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established ( Rookh et al . 1979 , Jordan et al . 1980 , Ottenweller & Hedge 1982 , Wong et al . 1983 , Kalsbeek et al . 2000 , Guo et al . 2015 ). Nerve fibres originating in the SCN innervating thyroid-releasing hormone (TRH) neurons in the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0111
Volume/Issue:
Volume 233: Issue 3
Open access
David R Grattan Centre for Neuroendocrinology and Department of Anatomy, Maurice Wilkins Centre for Molecular Biodiscovery, University of Otago, PO Box 913, Dunedin 9054, New Zealand
Centre for Neuroendocrinology and Department of Anatomy, Maurice Wilkins Centre for Molecular Biodiscovery, University of Otago, PO Box 913, Dunedin 9054, New Zealand

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the portal blood accounted for changes in prolactin secretion in various physiological conditions ( Ben-Jonathan et al . 1977 , 1980 , Gibbs & Neill 1978 , De Greef & Neill 1979 ). Dopamine receptors were identified on lactotroph cells in the

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-15-0213
Volume/Issue:
Volume 226: Issue 2
Open access
Shona Wood Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK

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Andrew Loudon Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK

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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

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-14-0141
Volume/Issue:
Volume 222: Issue 2
Open access
Alvaro Souto Padron 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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Ruy Andrade Louzada Neto 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
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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Thiago Urgal Pantaleão 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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Maria Carolina de Souza dos Santos 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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Renata Lopes Araujo 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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Bruno Moulin de Andrade 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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Monique da Silva Leandro 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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João Pedro Saar Werneck de Castro 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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Andrea Claudia Freitas Ferreira 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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Denise Pires de Carvalho 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

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0502
Volume/Issue:
Volume 221: Issue 3
Open access
Dominik Simon Botermann Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Nadine Brandes Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Anke Frommhold Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Ina Heß Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Alexander Wolff Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Arne Zibat Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Heidi Hahn Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Rolf Buslei Institute of Pathology, Sozialstiftung Bamberg, Klinikum am Bruderwald, Bamberg, Germany

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Anja Uhmann Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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binding of Hh ligands (e.g. mammalian Sonic, Indian or Desert Hh) to the receptor protein Patched1 (Ptch). This releases the inhibition of Smoothened (Smo), which results in translocation of Smo into the primary cilium and nuclear translocation of

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0388
Volume/Issue:
Volume 248: Issue 3
Open access
Graham W Aberdeen Departments of Obstetrics, Gynecology, Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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Jeffery S Babischkin Departments of Obstetrics, Gynecology, Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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Gerald J Pepe Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Virginia, USA

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Eugene D Albrecht Departments of Obstetrics, Gynecology, Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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levels or action of estrogen are curtailed or reduced during human pregnancy, e.g. preterm birth, aromatase gene mutation, or endocrine disruptors that interfere with estrogen receptor action, lead to T2DM in offspring ( Hofman et al. 2004

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-23-0364
Volume/Issue:
Volume 262: Issue 1
Open access