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Gustavo W Fernandes
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Cintia B Ueta Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Tatiane L Fonseca Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Cecilia H A Gouveia Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Carmen L Lancellotti Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Patrícia C Brum Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Marcelo A Christoffolete Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Antonio C Bianco Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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Miriam O Ribeiro Presbyterian University Mackenzie – Biological Science, Institute of Science Biomedical – Morpho-Functional Sciences, Department of Cell and Developmental Biology, Department of Anatomy, Santa Casa – AFIP and Pathology, School of Physical Education and Sport, Federal University of ABC – Human and Natural Sciences Center, Division of Endocrinology, Ciências Biológicas e da Saúde, CCBS, São Paulo, SP, Brazil

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energy expenditure and address the current high prevalence of obesity. In mice, BAT develops during the 3-day window E16.5–18.5 ( Hall et al . 2010 ) and after birth can be activated by the sympathetic nervous system (SNS) through stimulation of β

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0526
Volume/Issue:
Volume 221: Issue 3
Free access
Samira Fargali Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA

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Thomas Scherer Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA

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Andrew C Shin Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA

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Masato Sadahiro Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA

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Christoph Buettner Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA
Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA

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Stephen R Salton Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA
Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA

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Introduction The sympathetic nervous system (SNS) is an important regulator of glucose and fat metabolism, and its dysfunction can predispose to obesity and type 2 diabetes mellitus. The melanocortin pathway projects from the hypothalamic

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0172
Volume/Issue:
Volume 215: Issue 2
Free access
B Anguiano Instituto de Neurobiología, UNAM-Juriquilla, Querétaro, México 76230

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R Rojas-Huidobro Instituto de Neurobiología, UNAM-Juriquilla, Querétaro, México 76230

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G Delgado Instituto de Neurobiología, UNAM-Juriquilla, Querétaro, México 76230

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C Aceves Instituto de Neurobiología, UNAM-Juriquilla, Querétaro, México 76230

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sympathetic nervous system (SNS) and prolactin (PRL) have been frequently implicated as synergistic and antagonistic influences upon the effects of TH and viceversa. TH antagonizes PRL action by inhibiting the synthesis of the signal transducer and activator

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.05711
Volume/Issue:
Volume 183: Issue 2
Free access
Iyad H Manaserh Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA
Center for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA

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Emily Maly Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA

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Marziyeh Jahromi Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA

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Lakshmikanth Chikkamenahalli Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA

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Joshua Park Department of Neuroscience, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA

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Jennifer Hill Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA
Center for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, Ohio, USA

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nonshivering thermogenesis ( Oelkrug et al. 2015 ). The sympathetic nervous system (SNS) plays a large role in this process. The SNS activates BAT B3-adrenergic receptors causing higher UCP1 activity and UCP1 gene expression while increasing lipolysis in

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0052
Volume/Issue:
Volume 247: Issue 1
Restricted access
Liisa Ailanen Institute of Biomedicine and Turku Center for Disease Modelling; Drug Research Doctoral Program, University of Turku, Turku, Finland

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Suvi T Ruohonen Institute of Biomedicine and Turku Center for Disease Modelling, University of Turku, Turku, Finland

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Laura H Vähätalo Institute of Biomedicine and Turku Center for Disease Modelling, University of Turku, Turku, Finland

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Katja Tuomainen Institute of Biomedicine and Turku Center for Disease Modelling, University of Turku, Turku, Finland

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Kim Eerola Institute of Biomedicine and Turku Center for Disease Modelling, University of Turku, Turku, Finland

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Henriikka Salomäki-Myftari Institute of Biomedicine and Turku Center for Disease Modelling; Drug Research Doctoral Program, University of Turku, Turku, Finland

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Matias Röyttä Department of Pathology, University of Turku and Turku University Hospital, Turku, Finland

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Asta Laiho Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

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Markku Ahotupa Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland

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Helena Gylling Department of Internal Medicine, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland

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Eriika Savontaus Institute of Biomedicine and Turku Center for Disease Modelling, University of Turku; Turku University Hospital, Unit of Clinical Pharmacology, Turku, Finland

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(WAT) (Egawa et al. 1991, Zarjevski et al. 1993, Shi et al. 2013). An important source of NPY in the periphery is the sympathetic nervous system (SNS), and NPY levels are increased upon stress (Ekblad et al. 1984). Consistently, NPY has been

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0223
Volume/Issue:
Volume 234: Issue 1
Free access
Michael Rosenbaum Division of Molecular Genetics, Departments of Pediatrics and Medicine, College of Physicians and Surgeons, Columbia University, Russ Berrie Medical Science Pavilion, 6th Floor, 1150 St Nicholas Avenue, New York, New York 10032, USA

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Rudolph L Leibel Division of Molecular Genetics, Departments of Pediatrics and Medicine, College of Physicians and Surgeons, Columbia University, Russ Berrie Medical Science Pavilion, 6th Floor, 1150 St Nicholas Avenue, New York, New York 10032, USA

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↑GH Autonomics ↑↑PNS and ↓↓SNS ↑PNS and ↓SNS a Energy intake ↓↓Satiation Less↓↓Satiation a ↑Hunger a Less↑Hunger a REE, resting energy expenditure; NREE, non-resting energy expenditure; RER, respiratory exchange ratio; T 3 , triiodothyronine; T 4

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-14-0358
Volume/Issue:
Volume 223: Issue 1
Free access
Liping Luo Department of Metabolism and Endocrinology, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, 
Central South University, Changsha, Hunan, China

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Meilian Liu Department of Metabolism and Endocrinology, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, 
Central South University, Changsha, Hunan, China
Department of Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, 
Albuquerque, New Mexico, USA

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during fasting is also responsible for the activation of cAMP-dependent protein kinase A (PKA) pathway and lipolysis in adipocytes. Meanwhile, catecholamine released by sympathetic nervous system (SNS) is also stimulated by fasting, binds to β

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-16-0211
Volume/Issue:
Volume 231: Issue 3
Free access
Patricia C Lisboa Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551‐031, Brazil

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Ellen P S Conceição Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551‐031, Brazil

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Elaine de Oliveira Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551‐031, Brazil

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Egberto G Moura Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551‐031, Brazil

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dissipate energy and generate heat in rodents. The ablation of UCP1 gene is able to induce obesity without hyperphagia ( Lowell et al . 1993 ). The UCP1 mRNA expression is stimulated by the sympathetic nervous system (SNS) and leptin via the SNS ( Commins

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0237
Volume/Issue:
Volume 226: Issue 3
Free access
David E Henley Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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Fiona Buchanan Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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Rosemary Gibson Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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Jennie A Douthwaite Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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Susan A Wood Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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Wolfram W Woltersdorf Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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James R Catterall Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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Stafford L Lightman Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK

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system (SNS) hyperactivity is well documented in OSA with high sympathetic drive present across the 24-h period, even during daytime wakefulness and there is a reduction following CPAP ( Narkiewicz & Somers 2003 ). Chronic SNS activation may indirectly

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0245
Volume/Issue:
Volume 203: Issue 1
Free access
Eric D Bruder Endocrine Research Laboratory, St Luke’s Medical Center, Milwaukee, Wisconsin 53215, USA
Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA
Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA

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Lauren Jacobson Endocrine Research Laboratory, St Luke’s Medical Center, Milwaukee, Wisconsin 53215, USA
Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA
Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA

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Hershel Raff Endocrine Research Laboratory, St Luke’s Medical Center, Milwaukee, Wisconsin 53215, USA
Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA
Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA

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. 2004 ). Catecholamine release from the sympathetic nervous system (SNS) may be a mediator of these responses ( Young 2000 ). A previous study found that the transcription of the human leptin gene is activated by hypoxia, via the transcription factor

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06159
Volume/Issue:
Volume 185: Issue 3
Free access