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Francesca Spiga
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Louise R Harrison
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Susan A Wood
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Cliona P MacSweeney Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Organon Laboratories Limited, Organon Laboratories Limited, University of Bristol, Whitson Street, Bristol BS1 3NY, UK

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Fiona J Thomson Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Organon Laboratories Limited, Organon Laboratories Limited, University of Bristol, Whitson Street, Bristol BS1 3NY, UK

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Mark Craighead Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Organon Laboratories Limited, Organon Laboratories Limited, University of Bristol, Whitson Street, Bristol BS1 3NY, UK

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Morag Grassie Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Organon Laboratories Limited, Organon Laboratories Limited, University of Bristol, Whitson Street, Bristol BS1 3NY, UK

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Stafford L Lightman
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HPA axis in depression ( Dinan 1994 ) and chronic fatigue syndrome ( Demitrack et al . 1991 ) could be due to alterations in the mechanisms through which glucocorticoids, secreted by the adrenal cortex, exert inhibitory negative feedback effects on

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Louise Grahnemo Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Caroline Jochems Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden
Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Annica Andersson Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Cecilia Engdahl Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden
Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Claes Ohlsson Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Ulrika Islander Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Hans Carlsten Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden

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Introduction Glucocorticoids are frequently used for the treatment of noninfectious and autoimmune inflammation as, amongst other mechanisms, they can suppress lymphocytes ( Chantler et al . 2003 , Busillo & Cidlowski 2013 ). Prolonged use of

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E P S Conceição Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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E G Moura Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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A C Manhães Laboratory of Neurophysiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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J C Carvalho Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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J L Nobre Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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E Oliveira Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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P C Lisboa Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil

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identification of potential therapies ( Crane et al. 2015 , Yao et al. 2015 , Maksimov et al. 2016 ). Obesity is related, either as a cause or as a consequence, to the disruption of several hormonal systems. Higher levels of glucocorticoids (GCs) and

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Junny Chan
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Elizabeth H Rabbitt
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Barbara A Innes
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Judith N Bulmer
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Paul M Stewart
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Mark D Kilby
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Martin Hewison
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influences, which can modulate fetal development and lead to permanent alterations in the cardiovascular system: these are under nutrition and overexposure to glucocorticoids ( Seckl & Meaney 2004 ). Evidence that overexposure of the fetus to

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AC Wikstrom
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Glucocorticoids are widely used to treat inflammatory and malignant diseases. However, many individuals show a lack of therapeutic response and unwanted side-effects. Various known and unknown parameters determine glucocorticoid responsiveness, among them glucocorticoid receptor (GR)-interacting proteins. Several of the proteins interacting with GR also participate in other signal transduction pathways such as the AP-1 pathway and the nuclear factor-kappaB pathway. We suggest that a closer study of GR-interacting proteins may shed new light on mechanisms determining glucocorticoid sensitivity. In this commentary, the general mechanisms of GR action will be addressed and a proteomic-based method to study GR-interacting proteins will be described in brief.

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K L Davies Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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E J Camm Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK
The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Australia

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D J Smith Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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O R Vaughan Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK
Institute for Women’s Health, University College London, London, UK

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A J Forhead Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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A J Murray Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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A L Fowden Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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Introduction In adults, glucocorticoids are stress hormones with metabolic actions on a wide range of tissues that maintain functions critical to survival in adverse environmental conditions and during normal physiological challenges to

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Eva M G Viho Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands

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Jan Kroon Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA

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Richard A Feelders Department of Internal Medicine, Division of Endocrinology, Erasmus Medical Center, Rotterdam, the Netherlands

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René Houtman Precision Medicine Lab, Oss, the Netherlands

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Elisabeth S R van den Dungen Department of Internal Medicine, Division of Endocrinology, Erasmus Medical Center, Rotterdam, the Netherlands

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Alberto M Pereira Department of Endocrinology and Metabolism, Amsterdam University Medical Center, Amsterdam, the Netherlands

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Hazel J Hunt Corcept Therapeutics, Menlo Park, CA, USA

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Leo J Hofland Department of Internal Medicine, Division of Endocrinology, Erasmus Medical Center, Rotterdam, the Netherlands

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Onno C Meijer Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA

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Introduction Glucocorticoid (GC) stress hormones are essential for physiology and exert numerous functions via binding to the glucocorticoid receptor (GR). The predominant active GC hormone is cortisol in humans, while rats and mice adrenals

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Claire E Hills Department of Biological Sciences, Department of Infection, Biomedical Research Institute, The University of Warwick, Coventry CV4 7AL, UK

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Paul E Squires
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Rosemary Bland
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glucocorticoid regulated kinase-1 (SGK1). This short commentary looks at SGK1 pathophysiology and discusses the consequences of disturbed SGK1-mediated Na + reabsorption in diabetes in relation to the development of diabetic nephropathy. SGK1 The serum and

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K L Franko Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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A J Forhead Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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A L Fowden Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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programming of postnatal metabolism has been demonstrated in a number of species using a range of different techniques to induce intrauterine growth restriction (IUGR) including maternal stress and glucocorticoid administration (see McMillen & Robinson 2005

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Isabelle Vögeli
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Hans H Jung Department of Nephrology, Department of Neurology, Department of Medicine, Department of Internal Medicine, Prince Henry's Institute, Hypertension and Clinical Pharmacology, University Hospital Berne, CH-3010 Berne, Switzerland

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Bernhard Dick
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Sandra K Erickson Department of Nephrology, Department of Neurology, Department of Medicine, Department of Internal Medicine, Prince Henry's Institute, Hypertension and Clinical Pharmacology, University Hospital Berne, CH-3010 Berne, Switzerland

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Robert Escher Department of Nephrology, Department of Neurology, Department of Medicine, Department of Internal Medicine, Prince Henry's Institute, Hypertension and Clinical Pharmacology, University Hospital Berne, CH-3010 Berne, Switzerland

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John W Funder Department of Nephrology, Department of Neurology, Department of Medicine, Department of Internal Medicine, Prince Henry's Institute, Hypertension and Clinical Pharmacology, University Hospital Berne, CH-3010 Berne, Switzerland

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Felix J Frey
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Geneviève Escher
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pronounced hepatomegaly ( Repa et al . 2000 , Honda et al . 2001 , Dubrac et al . 2005 ). The intracellular concentrations of glucocorticoids are modulated by the 11β-hydroxysteroid dehydrogenase (HSD11B) enzyme. HSD11B type 1 (HSD11B1) preferentially

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