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M J F Newson Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), School of Clinical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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G R Pope Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), School of Clinical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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E M Roberts Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), School of Clinical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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S J Lolait Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), School of Clinical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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A-M O'Carroll Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), School of Clinical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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multiple homeostatic perturbations. These include regulation of fluid ( O'Carroll & Lolait 2003 ) and cardiovascular homeostasis ( Ishida et al . 2004 ), the stress response ( O'Carroll et al . 2003 ), food intake ( Taheri et al . 2002 ), gastric cell

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0375
Volume/Issue:
Volume 216: Issue 1
Open access
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Saadia Basharat
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Jennifer A Parker Division of Diabetes, University College London, Brunel University, Endocrinology and Metabolism, Department of Investigative Medicine, Imperial College London, Hammersmith Hospital Campus, 6th Floor, Commonwealth Building, Du Cane Road, London W12 0NN, UK

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Kevin G Murphy
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Stephen R Bloom
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Julia C Buckingham Division of Diabetes, University College London, Brunel University, Endocrinology and Metabolism, Department of Investigative Medicine, Imperial College London, Hammersmith Hospital Campus, 6th Floor, Commonwealth Building, Du Cane Road, London W12 0NN, UK

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Christopher D John
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inhibitory role in the regulation of the HPA axis ( Maffei et al . 1995 ). Leptin administration blunts the restraint stress-induced activation of the HPA axis in mice ( Heiman et al . 1997 ) and can directly inhibit ACTH-stimulated cortisol

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0249
Volume/Issue:
Volume 221: Issue 2
Open access
R Prasad Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK

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J C Kowalczyk Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK

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E Meimaridou Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK

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H L Storr Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK

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L A Metherell Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK

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, differentiation, apoptosis, immune regulation and cellular adaptation to stress ( Ray et al . 2012 , Sena & Chandel 2012 ). A critical balance in redox status needs to be maintained and this is achieved by numerous interacting antioxidant pathways. Oxidative

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0346
Volume/Issue:
Volume 221: Issue 3
Open access
Ying Sze Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, UK
The Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, UK

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Joana Fernandes The Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, UK

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Zofia M Kołodziejczyk Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, UK

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Paula J Brunton Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, UK
The Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, UK
Zhejiang University-University of Edinburgh Institute, International Campus, Haining, Zhejiang, P.R. China

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Introduction Stress experienced during pregnancy has detrimental effects on the offspring across the life course, beginning during fetal development, persisting through the postnatal period and into adulthood ( Glover et al. 2018 ). This

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-22-0226
Volume/Issue:
Volume 255: Issue 3
Open access
Bernadette M Trojanowski Institute of Physiological Chemistry, Ulm University, Ulm, Germany

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Heba H Salem Faculty of Pharmacy, Cairo University, Cairo, Egypt
Faculty of Pharmacy, King Khalid University, Abha, Saudi Arabia

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Heike Neubauer Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany

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Eric Simon Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany

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Martin Wagner Division of Endocrinology, Diabetes and Metabolism, Ulm University Medical Centre, Ulm University, Ulm, Germany

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Rajkumar Dorajoo Genome Institute of Singapore, Agency for Science Technology and Research, Singapore, Singapore

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Bernhard O Boehm Lee Kong Chiang School of Medicine, Nanyang Technological University, Singapore, Singapore
Imperial College London, London, UK

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Leticia Labriola Institute of Physiological Chemistry, Ulm University, Ulm, Germany
Department of Biochemistry, University of São Paulo, São Paulo, Brazil

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Thomas Wirth Institute of Physiological Chemistry, Ulm University, Ulm, Germany

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Bernd Baumann Institute of Physiological Chemistry, Ulm University, Ulm, Germany

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early diabetes onset in MODY4 mutation carriers ( Fajans et al. 2010 ). In this condition β-cells are stressed and forced to compensate the increased insulin demand ( Ferrannini et al. 2004 ). Thus, the occurrence of any additional β-cell stress

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0208
Volume/Issue:
Volume 244: Issue 2
Open access
Joachim M Weitzel Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Torsten Viergutz Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Dirk Albrecht Institute of Microbiology, Ernst-Moritz-Arndt-University, Greifswald, Germany

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Rupert Bruckmaier Veterinary Physiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland

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Marion Schmicke Clinic for Cattle, Endocrinology Laboratory, University of Veterinary Medicine Hannover, Hannover, Germany

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Armin Tuchscherer Institute of Genetics and Biometry, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Franziska Koch Institute of Nutritional Physiology ‘Oskar Kellner’, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Björn Kuhla Institute of Nutritional Physiology ‘Oskar Kellner’, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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the summer period induce metabolic heat stress, which has adverse effects on milk production, reproductive performance and animal welfare issues, among others. Counterregulatory mechanisms generally include an increased sweating rate, increased water

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0066
Volume/Issue:
Volume 234: Issue 2
Open access
David O'Regan Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Christopher J Kenyon Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Jonathan R Seckl Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Megan C Holmes Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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excess glucocorticoids via maternal stress, inhibition of placental 11β-hydroxysteroid dehydrogenase type 2, the normal ‘barrier’ to maternal glucocorticoids, or its bypass with non-substrate synthetic glucocorticoids, such as dexamethasone (DEX

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0327
Volume/Issue:
Volume 196: Issue 2
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Carolina Gaudenzi Neuro-Epigenetics Research Group, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom

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Karen R Mifsud Neuro-Epigenetics Research Group, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom

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Johannes M H M Reul Neuro-Epigenetics Research Group, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom

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brain homeostasis, whilst the GR is predominantly involved in phasic actions mediating stress- and circadian-related GC responses ( Reul et al. 1987 ). More recently, however, this view has been adjusted. Using MR and GR chromatin immunoprecipitation

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-22-0293
Volume/Issue:
Volume 258: Issue 2
Open access
Miroslav Adzic
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Jelena Djordjevic
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Ana Djordjevic
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Ana Niciforovic
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Constantinos Demonacos Laboratory of Molecular Biology and Endocrinology, School of Pharmacy, Faculty of Life Sciences, VINCA Institute of Nuclear Sciences, PO Box-522-MBE090, 11001 Belgrade, Serbia

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Marija Radojcic
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Marija Krstic-Demonacos Laboratory of Molecular Biology and Endocrinology, School of Pharmacy, Faculty of Life Sciences, VINCA Institute of Nuclear Sciences, PO Box-522-MBE090, 11001 Belgrade, Serbia

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Introduction Response to neuroendocrine stress begins with the activation of the hypothalamic–pituitary–adrenal (HPA) axis leading to the increase in stress hormones glucocorticoids (GCs). These hormones mediate adaptation to stress and also

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0509
Volume/Issue:
Volume 202: Issue 1
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Neil Tanday Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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Aimee Coulter-Parkhill Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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R Charlotte Moffett Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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Karthick Suruli Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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Vaibhav Dubey Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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Peter R Flatt Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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Nigel Irwin Diabetes Research Centre, Ulster University, Coleraine, Londonderry, Northern Ireland

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of mature islet cells and ability of alpha cells to function as progenitors for insulin positive beta cells through distinct lineage alteration ( Tanday et al. 2020 b ). Moreover, alpha cells are innately more resistant to oxidative stress and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-23-0174
Volume/Issue:
Volume 259: Issue 2
Open access