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

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J Miles Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK

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E J Camm Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, 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, Downing Street, Cambridge, UK

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P Barker MRC Metabolic Diseases Unit, Mouse Biochemistry Laboratory, Cambridge Biomedical Campus, Cambridge, UK

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K Taylor Endocrine Laboratory, Blood Sciences, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge, UK

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

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

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) However, relatively little is known about the long-term effects of naturally occurring increments in fetal cortisol concentrations of the magnitude seen in response to prenatal environmental challenges known to programme adult metabolic and endocrine

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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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study in fetal sheep has demonstrated that the natural prepartum cortisol surge closely parallels the increase in mitochondrial OXPHOS capacity of skeletal muscle towards term ( Davies et al. 2020 ). However, whether these changes are the direct

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Lesley A Hill Departments of Cellular and Physiological Sciences and Obstetrics and Gynaecology, The University of British Columbia, Vancouver, British Columbia, Canada

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Dimitra A Vassiliadi Endocrine Unit, Second Department of Internal Medicine-Research Institute and Diabetes Center, Attiko University Hospital, Athens, Greece

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Ioanna Dimopoulou Endocrine Unit, Second Department of Internal Medicine-Research Institute and Diabetes Center, Attiko University Hospital, Athens, Greece

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Anna J Anderson BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Luke D Boyle BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Alixe H M Kilgour BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Roland H Stimson BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Yoan Machado Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, British Columbia, Canada

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Christopher M Overall Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, British Columbia, Canada

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Brian R Walker BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom

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John G Lewis Canterbury Health Laboratories, Christchurch, New Zealand

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Geoffrey L Hammond Departments of Cellular and Physiological Sciences and Obstetrics and Gynaecology, The University of British Columbia, Vancouver, British Columbia, Canada

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(RIAs) correlate well with measurements of its cortisol-binding capacity, except in samples containing CBG variants with abnormal steroid-binding properties ( Robinson & Hammond 1985 , Smith et al. 1992 , Emptoz-Bonneton et al. 2000 , Perogamvros

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Laura L Gathercole Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Nikolaos Nikolaou Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Shelley E Harris Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Anastasia Arvaniti Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Toryn M Poolman Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Jonathan M Hazlehurst Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Denise V Kratschmar Swiss Centre for Applied Human Toxicology and Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland

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Marijana Todorčević Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Ahmad Moolla Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Niall Dempster Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Ryan C Pink Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Michael F Saikali Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada

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Liz Bentley Mammalian Genetics Unit, Medical Research Council Harwell, Oxford, UK

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Trevor M Penning Center of Excellence in Environmental Toxicology, Department of Systems Pharmacology & Translational Therapeutics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Claes Ohlsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Carolyn L Cummins Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada

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Matti Poutanen Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland

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Alex Odermatt Swiss Centre for Applied Human Toxicology and Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland

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Roger D Cox Mammalian Genetics Unit, Medical Research Council Harwell, Oxford, UK

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Jeremy W Tomlinson Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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described are 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) and the 5α-reductases type 1 and 2 (5αR1 and 2). 11β-HSD1 converts the inactive glucocorticoid cortisone to its active form cortisol, and 11β-Hsd1 –/– mice have a beneficial metabolic phenotype

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Ryun S Ahn
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Jee H Choi Graduate School of Integrative Medicine, Hormone Research Center, Department of Obstetrics and Gynecology, Department of Family Medicine, Department of Life sciences, Research Institute of Integrative Medicine, CHA Medical University, Yuksam‐dong 605, Kangnamgu, Seoul 135-907, Republic of Korea

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Bum C Choi Graduate School of Integrative Medicine, Hormone Research Center, Department of Obstetrics and Gynecology, Department of Family Medicine, Department of Life sciences, Research Institute of Integrative Medicine, CHA Medical University, Yuksam‐dong 605, Kangnamgu, Seoul 135-907, Republic of Korea

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Jung H Kim Graduate School of Integrative Medicine, Hormone Research Center, Department of Obstetrics and Gynecology, Department of Family Medicine, Department of Life sciences, Research Institute of Integrative Medicine, CHA Medical University, Yuksam‐dong 605, Kangnamgu, Seoul 135-907, Republic of Korea

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Sung H Lee Graduate School of Integrative Medicine, Hormone Research Center, Department of Obstetrics and Gynecology, Department of Family Medicine, Department of Life sciences, Research Institute of Integrative Medicine, CHA Medical University, Yuksam‐dong 605, Kangnamgu, Seoul 135-907, Republic of Korea

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Simon S Sung Graduate School of Integrative Medicine, Hormone Research Center, Department of Obstetrics and Gynecology, Department of Family Medicine, Department of Life sciences, Research Institute of Integrative Medicine, CHA Medical University, Yuksam‐dong 605, Kangnamgu, Seoul 135-907, Republic of Korea

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for a better assessment of the diurnal rhythm-mediated secretion of cortisol and sex steroids. The diurnal pattern of cortisol secretory activity is well characterized. Cortisol reaches a zenith around the time of awakening in the morning and a nadir

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Dawn E W Livingstone Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Emma M Di Rollo Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Chenjing Yang Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Lucy E Codrington Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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John A Mathews Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Madina Kara Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Katherine A Hughes Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Christopher J Kenyon Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Brian R Walker Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Ruth Andrew Endocrinology, Queen's Medical Research Institute, University and British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Introduction Activation of the hypothalamic–pituitary–adrenal (HPA) axis is a vital component of the stress response, driving production of glucocorticoid hormones (cortisol in humans, corticosterone in rodents) that mediate essential adaptations of

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I J Bujalska
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L L Gathercole
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J W Tomlinson
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C Darimont Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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J Ermolieff Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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A N Fanjul Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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P A Rejto Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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P M Stewart
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rate of 1. 0 ml/min. Under these experimental conditions, the retention time for cortisone and cortisol were 4.5 and 5.5 min respectively. The initial reaction velocities recorded were in the linear range and were determined by measuring the peak area

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K S Wilson The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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C S Tucker The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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E A S Al-Dujaili The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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M C Holmes The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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P W F Hadoke The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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C J Kenyon The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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M A Denvir The University/BHF Centre for Cardiovascular Science, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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-body cortisol to air stress. Although, theoretically, ethanol exposure could be a contributory factor in the current dexamethasone experiments, it should be noted that controls for these experiments were treated with similar concentrations of ethanol. Also

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S Khan Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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D E W Livingstone Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK
Centre for Discovery Brain Science, University of Edinburgh, Hugh Robson Building, Edinburgh, UK

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A Zielinska College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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C L Doig Department of Biosciences, School of Science & Technology, Nottingham Trent University, Nottingham, UK

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D F Cobice Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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C L Esteves Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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J T Y Man Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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N Z M Homer Mass Spectrometry Core Laboratory, Edinburgh Clinical Research Facility, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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J R Seckl Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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C L MacKay SIRCAMS, School of Chemistry, University of Edinburgh, Joseph Black Building, King's Buildings, Edinburgh, UK

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S P Webster Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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G G Lavery Department of Biosciences, School of Science & Technology, Nottingham Trent University, Nottingham, UK

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K E Chapman Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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B R Walker Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK
Clinical & Translational Research Institute, Newcastle University, International Centre for Life, Central Parkway, Newcastle upon Tyne, UK

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R Andrew Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK
Mass Spectrometry Core Laboratory, Edinburgh Clinical Research Facility, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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Introduction 11β-Hydroxysteroid dehydrogenase 1 (11βHSD1) generates active 11-hydroxy glucocorticoids (cortisol (human), corticosterone (rodent and human)) from intrinsically inert 11-keto steroids (cortisone, 11-dehydrocorticosterone (11DHC

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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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