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Taira Wada Laboratory of Health Science, School of Pharmacy, Nihon University, Funabshi, Chiba, Japan

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Yukiko Yamamoto Laboratory of Health Science, School of Pharmacy, Nihon University, Funabshi, Chiba, Japan

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Yukiko Takasugi Laboratory of Health Science, School of Pharmacy, Nihon University, Funabshi, Chiba, Japan

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Hirotake Ishii Laboratory of Health Science, School of Pharmacy, Nihon University, Funabshi, Chiba, Japan

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Taketo Uchiyama Laboratory of Organic Chemistry, School of Pharmacy, Nihon University, Funabshi, Chiba, Japan

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Kaori Saitoh Department of Psychiatry, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan

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Masahiro Suzuki Department of Psychiatry, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan

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Makoto Uchiyama Department of Psychiatry, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan
Tokyo Adachi Hospital, Adachi, Tokyo, Japan

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Hikari Yoshitane Department of Biological Sciences, School of Science, The University of Tokyo, Bunkyo-ku, Tokyo, Japan

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Yoshitaka Fukada Department of Biological Sciences, School of Science, The University of Tokyo, Bunkyo-ku, Tokyo, Japan

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Shigeki Shimba Laboratory of Health Science, School of Pharmacy, Nihon University, Funabshi, Chiba, Japan

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et al. 1999 ). Because adiponectin is a crucial factor in the regulation of glucose and lipid metabolism, inflammation, and oxidative stress, reduced adiponectin levels play a causal role in the development of insulin resistance, metabolic syndrome

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-22-0006
Volume/Issue:
Volume 254: Issue 2
Open access
Shiho Fujisaka First Department of Internal Medicine, Faculty of Medicine, University of Toyama, Sugitani, Toyama, Japan

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Yoshiyuki Watanabe First Department of Internal Medicine, Faculty of Medicine, University of Toyama, Sugitani, Toyama, Japan

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Kazuyuki Tobe First Department of Internal Medicine, Faculty of Medicine, University of Toyama, Sugitani, Toyama, Japan

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Physiological role of the gut microbiota Nutrient metabolism and absorption Degradation of indigestible polysaccharides Short-chain fatty acids (SCFAs) are metabolites generated from the fermentation of insoluble dietary fiber and

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-22-0111
Volume/Issue:
Volume 256: Issue 3
Open access
Craig L Doig School of Clinical and Experimental Medicine, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham B15 2TT, UK

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Jamila Bashir School of Clinical and Experimental Medicine, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham B15 2TT, UK

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Agnieszka E Zielinska School of Clinical and Experimental Medicine, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham B15 2TT, UK

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Mark S Cooper School of Clinical and Experimental Medicine, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham B15 2TT, UK

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Paul M Stewart School of Clinical and Experimental Medicine, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham B15 2TT, UK

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Gareth G Lavery School of Clinical and Experimental Medicine, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham B15 2TT, UK

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glucocorticoid metabolism in inflammatory arthritis . Annals of Rheumatic Disease 67 1204 – 1210 . ( doi:10.1136/ard.2008.090662 ) Ignatova ID Kostadinova RM Goldring CE Nawrocki AR Frey FJ Frey BM 2009 Tumor necrosis factor-α upregulates 11β

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0494
Volume/Issue:
Volume 220: Issue 3
Open access
Dawn E W Livingstone University/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK
Centre for Integrative Physiology, University of Edinburgh, Edinburgh, UK

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Emma M Di Rollo University/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Tracy C-S Mak University/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Karen Sooy University/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Brian R Walker University/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Ruth Andrew University/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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 Adrenal gland (mg) 2.3 ± 0.3 2.3 ± 0.3  Thymus (mg) 34.1 ± 2.3 34.9 ± 2.9  Plasma testosterone (pg/mL) 66 ± 10 123 ± 24* Liver glucocorticoid metabolism  11βHSD1 velocity (nmol/mg/h) 20.1 ± 2.3 16

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0125
Volume/Issue:
Volume 232: Issue 1
Open access
S J Brandt Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany
German Center for Diabetes Research (DZD), Neuherberg, Germany

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M Kleinert Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany
German Center for Diabetes Research (DZD), Neuherberg, Germany

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M H Tschöp Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany
German Center for Diabetes Research (DZD), Neuherberg, Germany
Division of Metabolic Diseases, Technische Universität, Munich, Germany

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T D Müller Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany
German Center for Diabetes Research (DZD), Neuherberg, Germany

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poor. A number of psychological and economic factors are involved in such compliance, and humans might be evolutionarily predisposed to a positive energy balance ( Wells 2006 ). Furthermore, once excess weight has been gained, human metabolism

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-18-0264
Volume/Issue:
Volume 238: Issue 2
Open access
Elisa Villalobos University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom

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Allende Miguelez-Crespo University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Ruth A Morgan University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
Scotland’s Rural College, The Roslin Institute, Easter Bush Campus, United Kingdom

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Lisa Ivatt University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Mhairi Paul University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Joanna P Simpson University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Natalie Z M Homer University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Dominic Kurian The Roslin Institute, Royal (Dick) School of Veterinary Studies, College of Medicine and Veterinary Medicine, University of Edinburgh, Easter Bush Campus, Edinburgh, United Kingdom

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Judit Aguilar The Roslin Institute, Royal (Dick) School of Veterinary Studies, College of Medicine and Veterinary Medicine, University of Edinburgh, Easter Bush Campus, Edinburgh, United Kingdom

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Rachel A Kline The Roslin Institute, Royal (Dick) School of Veterinary Studies, College of Medicine and Veterinary Medicine, University of Edinburgh, Easter Bush Campus, Edinburgh, United Kingdom

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Thomas M Wishart The Roslin Institute, Royal (Dick) School of Veterinary Studies, College of Medicine and Veterinary Medicine, University of Edinburgh, Easter Bush Campus, Edinburgh, United Kingdom

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Nicholas M Morton University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
Centre for Systems Health and Integrated Metabolic Research, Nottingham Trent University, Nottingham, United Kingdom

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Roland H Stimson University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Ruth Andrew University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Brian R Walker University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom

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Mark Nixon University/British Heart Foundation Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom

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Abcc1 -deficient mice on HFD, we explored other mechanisms that might explain their adverse glucose metabolism phenotype. Transcriptomic and proteomic analyses reveal differential responses to high-fat diet in adipose tissue from Abcc1 -deficient

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-24-0024
Volume/Issue:
Volume 262: Issue 2
Open access
David M Cartwright Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Lucy A Oakey Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Rachel S Fletcher Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Craig L Doig Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
School of Science and Technology, Nottingham Trent University, Nottingham, UK

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Silke Heising Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Dean P Larner Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Daniela Nasteska Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Caitlin E Berry Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Sam R Heaselgrave Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Christian Ludwig Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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David J Hodson Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Gareth G Lavery Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Antje Garten Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Pediatric Research Center, Hospital for Child and Adolescent Medicine, Leipzig University, Leipzig, Germany

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metabolic and mitochondrial disorders. Beneficial effects on energy metabolism and mitochondrial function were found in animal models of diet-induced obesity ( Yoshino et al. 2011 , Cantó et al. 2012 , Yoon et al. 2015 , Mills et al. 2016 , de

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-21-0123
Volume/Issue:
Volume 251: Issue 1
Open access
T V Novoselova Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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R Larder University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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D Rimmington University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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C Lelliott Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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E H Wynn Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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R J Gorrigan Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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P H Tate Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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L Guasti Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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The Sanger Mouse Genetics Project Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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S O’Rahilly University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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A J L Clark Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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D W Logan Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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A P Coll University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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L F Chan Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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metabolism, a function known to be regulated by melanocortins ( Nogueiras et al . 2007 , Perez-Tilve et al . 2010 ). In this study, we have used an independently derived line of Mrap2 -deficient mice ( Mrap2 tm1a/tm1a ) on two different genetic

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0057
Volume/Issue:
Volume 230: Issue 1
Open access
Dawn E W Livingstone Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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Sarah L Grassick Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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Gillian L Currie Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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

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

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supported the hypothesis that variations in glucocorticoid metabolism within target tissues play an important role in the pathophysiology of Metabolic Syndrome. In addition to 11β-HSD1, glucocorticoids are metabolised by several other enzymes ( Fig. 1 ). In

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0003
Volume/Issue:
Volume 201: Issue 2
Open access
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Margaret K Hahn Centre for Addiction and Mental Health, Toronto, Ontario, Canada
Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada
Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada
Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada
Banting & Best Diabetes Centre, Toronto, Ontario, Canada

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Adria Giacca Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada
Banting & Best Diabetes Centre, Toronto, Ontario, Canada
Department of Physiology, University of Toronto, Toronto, Ontario, Canada

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Sandra Pereira Centre for Addiction and Mental Health, Toronto, Ontario, Canada
Department of Physiology, University of Toronto, Toronto, Ontario, Canada

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Introduction Breakthroughs in metabolic research rely upon in vivo studies using animal models, usually rodents. Assessment of glucose metabolism in rodents is a key component of diabetes research. Although general guidelines for

Article Type:
Review Article
Collections:
Insulin resistance and type 2 diabetes mellitus
DOI:
https://doi.org/10.1530/JOE-23-0308
Volume/Issue:
Volume 260: Issue 3
Open access