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Alexander V Amram Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Stephen Cutie Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Guo N Huang Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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their contributions to the evolutionarily divergent potentials of CM proliferation and heart regeneration, including thyroid hormone, vitamin D, and glucocorticoids. A recent phylogenetic analysis of CM ploidy, a proxy of cardiac regenerative potential

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-20-0503
Volume/Issue:
Volume 10: Issue 1
Open access
Huifei Sophia Zheng Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Jeffrey G Daniel Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Julia M Salamat Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Laci Mackay Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Chad D Foradori Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Robert J Kemppainen Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Satyanarayana R Pondugula Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Ya-Xiong Tao Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Chen-Che Jeff Huang Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Introduction Glucocorticoids (GCs) are primary stress hormones and critical regulators of several physiological mechanisms. GCs commonly elicit their function through glucocorticoid receptor (GR)-mediated genomic effects. However, these

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0064
Volume/Issue:
Volume 11: Issue 8
Open access
Angelica Sharma Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Katharine Lazarus Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Deborah Papadopoulou Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Hemanth Prabhudev Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Tricia Tan Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, North West London Pathology, London, UK

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Karim Meeran Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Sirazum Choudhury Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, North West London Pathology, London, UK

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Introduction Patients with adrenal insufficiency (AI) have premature morbidity and mortality ( 1 ). Mildly elevated levels of glucocorticoids or non-circadian timing of therapy may contribute towards cardiovascular disease and increased

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-23-0097
Volume/Issue:
Volume 12: Issue 8
Open access
Kerry V Fanson Wildlife Reproductive Centre, School of Life and Environmental Sciences, School of Agriculture and Food Sciences, Taronga Conservation Society Australia, Dubbo, New South Wales, Australia
Wildlife Reproductive Centre, School of Life and Environmental Sciences, School of Agriculture and Food Sciences, Taronga Conservation Society Australia, Dubbo, New South Wales, Australia

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Tamara Keeley Wildlife Reproductive Centre, School of Life and Environmental Sciences, School of Agriculture and Food Sciences, Taronga Conservation Society Australia, Dubbo, New South Wales, Australia
Wildlife Reproductive Centre, School of Life and Environmental Sciences, School of Agriculture and Food Sciences, Taronga Conservation Society Australia, Dubbo, New South Wales, Australia

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Benjamin G Fanson Wildlife Reproductive Centre, School of Life and Environmental Sciences, School of Agriculture and Food Sciences, Taronga Conservation Society Australia, Dubbo, New South Wales, Australia

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Introduction Elevated glucocorticoid (GC) titers associated with chronic stress can lead to reproductive failure (1) . Consequently, studies of reproductive dysfunction often focus on the suppressive effects of GCs. However, GCs also play a

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-14-0025
Volume/Issue:
Volume 3: Issue 2
Open access
Riccardo Pofi Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism and NIHR Oxford Biomedical Research Centre, Churchill Hospital, University of Oxford, Oxford, UK

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Ilaria Bonaventura Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena, Rome, Italy

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Joanne Duffy Department of Clinical Chemistry and Immunology, Heartlands Hospital, Birmingham, UK

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Zoe Maunsell Department of Clinical Biochemistry, Oxford University Hospitals NHS Foundation Trust, Oxford, UK

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Brian Shine Department of Clinical Biochemistry, Oxford University Hospitals NHS Foundation Trust, Oxford, UK

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Andrea M Isidori Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena, Rome, Italy

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

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Introduction Primary adrenal insufficiency (PAI) is a rare disease consisting of the inability of the adrenal cortex to produce adequate levels of glucocorticoids (GCs), with or without concomitant inadequate production of mineralocorticoids

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-23-0059
Volume/Issue:
Volume 12: Issue 9
Open access
Thomas Reinehr Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Alexandra Kulle Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University Hospital of Schleswig – Holstein, UKSH, Campus Kiel/Christian Albrechts University of Kiel, CAU, Kiel, Germany

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Juliane Rothermel Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Caroline Knop-Schmenn Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Nina Lass Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Christina Bosse Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Paul-Martin Holterhus Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University Hospital of Schleswig – Holstein, UKSH, Campus Kiel/Christian Albrechts University of Kiel, CAU, Kiel, Germany

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regulation of precursors of androgens and other steroid hormones within the steroid metabolome encompassing glucocorticoids, mineralocorticoids and estrogens is largely unknown in PCOS. Although PCOS has frequently been reported in adolescents, the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0051
Volume/Issue:
Volume 6: Issue 4
Open access
Hanna F Nowotny Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Jillian Bryce Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Salma R Ali Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Roberta Giordano Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
Division of Endocrinology, Diabetes and Metabolism, Department of Medical Sciences, University of Turin, Turin, Italy

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Federico Baronio Pediatric Unit, Department Hospital of Woman and Child, Endo-ERN Centre IT11, IRCSS AOU S.Orsola-Malpighi University Hospital, Bologna, Italy

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Irina Chifu Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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Lea Tschaidse Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Martine Cools Department of Paediatric Endocrinology, Ghent University Hospital, University of Ghent, Ghent, Belgium

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Erica LT van den Akker Department of Pediatrics, Division of Pediatric Endocrinology, Erasmus MC - Sophia Children’s Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands

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Henrik Falhammar Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden

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Natasha M Appelman-Dijkstra Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Luca Persani Department of Endocrine and Metabolic Diseases, Istituto Auxologico Italiano IRCCS, Milan, Italy
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan Italy

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Guglielmo Beccuti Department of Clinical and Biological Sciences, University of Turin, Turin, Italy

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Ian L Ross Division of Endocrinology, Department of Medicine, University of Cape Town, Cape Town, South Africa

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Simona Grozinsky-Glasberg Neuroendocrine Tumor Unit, ENETS Center of Excellence, Department of Endocrinology and Metabolism, Hadassah Medical Organisation and Faculty of Medicine, the Hebrew University, Jerusalem, Israel

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Alberto M Pereira Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Eystein S Husebye Department of Clinical Science and KG Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Department of Medicine, Karolinska Institutet, Stockholm, Sweden

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Stefanie Hahner Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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S Faisal Ahmed Office for Rare Conditions, University of Glasgow, Glasgow, UK
Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom

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Nicole Reisch Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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AI and long-term glucocorticoid substitution therapy or glucocorticoid excess in Cushing’s syndrome (CS), are regularly prone to infections, especially those of the upper airways and gastrointestinal tract, due to impaired immune cell function ( 17

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0416
Volume/Issue:
Volume 12: Issue 4
Open access
Alexander Tacey Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Department of Medicine-Western Health, Australian Institute for Musculoskeletal Science (AIMSS), Melbourne Medical School, The University of Melbourne, Melbourne, Victoria, Australia

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Lewan Parker Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Institute for Physical Activity and Nutrition, Deakin University, Geelong, Victoria, Australia

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Bu B Yeap Medical School, University of Western Australia, and Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, Western Australia, Australia

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John Joseph PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

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Ee M Lim PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

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Andrew Garnham Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia

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David L Hare University of Melbourne and the Department of Cardiology, Austin Health, Melbourne, Victoria, Australia

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Tara Brennan-Speranza Department of Physiology and Bosch Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia

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Itamar Levinger Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Department of Medicine-Western Health, Australian Institute for Musculoskeletal Science (AIMSS), Melbourne Medical School, The University of Melbourne, Melbourne, Victoria, Australia

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Introduction Glucocorticoids (GC) are a naturally occurring catabolic steroid, produced by the hypothalamic–pituitary–adrenal (HPA) axis and regulated by neuroendocrine and immune responses ( 1 , 2 ). Synthetic forms of GC, such as

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-18-0473
Volume/Issue:
Volume 8: Issue 2
Open access
Legh Wilkinson Department of Biochemistry, Stellenbosch University, Stellenbosch, South Africa

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Nicolette J D Verhoog Department of Biochemistry, Stellenbosch University, Stellenbosch, South Africa

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Ann Louw Department of Biochemistry, Stellenbosch University, Stellenbosch, South Africa

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pathway of the stress response ( 1 ). This in turn, has many peripheral effects, such as an increase in circulating glucocorticoids (GCs) ( 2 , 3 ). Chronic stress or prolonged exogenous GC treatment also disrupts the central homeostatic nature of GC

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-18-0421
Volume/Issue:
Volume 7: Issue 12
Open access
Peter Ergang Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Anna Mikulecká Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Martin Vodicˇka Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic

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Karla Vagnerová Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Ivan Mikšík Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Jirˇí Pácha Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic

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the sympathetic–adrenal–medullary axis, which subsequently release glucocorticoids and catecholamines, respectively. The HPA and SNS axes are the two major pathways through which stress is able to modulate immune functions depending on the nature

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-18-0319
Volume/Issue:
Volume 7: Issue 12
Open access