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Cátia F Gonçalves Wellcome Centre for Cell Matrix Research, Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK

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Qing-Jun Meng Wellcome Centre for Cell Matrix Research, Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK

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their precise spatial and temporal control. Remarkably, physiological functions such as longitudinal bone growth, bone remodelling, chondrocyte metabolism and cartilage matrix turnover exhibit 24-h rhythms, being controlled by the peripheral circadian

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-19-0256
Volume/Issue:
Volume 243: Issue 3
Free access
Anjara Rabearivony School of Life Sciences and Technology, China Pharmaceutical University, Nanjing, China

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Huan Li School of Life Sciences and Technology, China Pharmaceutical University, Nanjing, China

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Shiyao Zhang School of Life Sciences and Technology, China Pharmaceutical University, Nanjing, China

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Siyu Chen School of Life Sciences and Technology, China Pharmaceutical University, Nanjing, China

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Xiaofei An Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China

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Chang Liu School of Life Sciences and Technology, China Pharmaceutical University, Nanjing, China

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styles would abolish normal hepatic rhythmicity, leading to metabolic diseases ( Ferrell & Chiang 2015 ). Hepatic metabolism responds sensitively to external changes. For instance, thermoneutral housing (30°C) exacerbates nonalcoholic fatty liver

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0100
Volume/Issue:
Volume 247: Issue 2
Free 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
Sharon H Chou Section of Adult and Pediatric Endocrinology, Division of Endocrinology, Section of Endocrinology, Diabetes and Metabolism, The University of Chicago, 5841 South Maryland Avenue, MC 1027, Chicago, Illinois 60637, USA

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Christos Mantzoros Section of Adult and Pediatric Endocrinology, Division of Endocrinology, Section of Endocrinology, Diabetes and Metabolism, The University of Chicago, 5841 South Maryland Avenue, MC 1027, Chicago, Illinois 60637, USA
Section of Adult and Pediatric Endocrinology, Division of Endocrinology, Section of Endocrinology, Diabetes and Metabolism, The University of Chicago, 5841 South Maryland Avenue, MC 1027, Chicago, Illinois 60637, USA

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syndrome, and other neuroendocrine abnormalities as well as deficits in bone metabolism and immune function ( Chan et al . 2003 , Chan & Mantzoros 2005 , Dardeno et al . 2010 ). Congenital leptin deficiency Patients with complete leptin deficiency due

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-14-0245
Volume/Issue:
Volume 223: Issue 1
Free access
Hongying An Divisions of Metabolism and Endocrinology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, Maryland 21287, USA

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Ling He Divisions of Metabolism and Endocrinology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, Maryland 21287, USA

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its AMP-activation property and its role in regulating three key enzymes in lipid metabolism ( Brown et al. 1975 , Hardie et al. 1989 ). Over the past decades, numerous studies have confirmed the function of AMPK as a principal energy sensor of

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-15-0447
Volume/Issue:
Volume 228: Issue 3
Free access
Oliver C Watkins Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Mohammed Omedul Islam Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Preben Selvam Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Reshma Appukuttan Pillai Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Amaury Cazenave-Gassiot Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
Singapore Lipidomics Incubator, Life Sciences Institute, National University of Singapore, Singapore, Singapore

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Anne K Bendt Singapore Lipidomics Incubator, Life Sciences Institute, National University of Singapore, Singapore, Singapore

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Neerja Karnani Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research, Singapore, Singapore

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Keith M Godfrey MRC Lifecourse Epidemiology Unit and NIHR Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, UK

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Rohan M Lewis MRC Lifecourse Epidemiology Unit and NIHR Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, UK

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Markus R Wenk Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
Singapore Lipidomics Incubator, Life Sciences Institute, National University of Singapore, Singapore, Singapore

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Shiao-Yng Chan Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research, Singapore, Singapore

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et al. 2016 ). Perturbations in myo-inositol synthesis, metabolism and excretion have been associated with the insulin-resistant conditions of polycystic ovary syndrome (PCOS), diabetes mellitus and metabolic syndrome ( Croze & Soulage 2013 ), and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0267
Volume/Issue:
Volume 243: Issue 1
Free access
Emily J King Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia
Central Clinical School, Monash University, Melbourne, Victoria, Australia

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Simon T Bond Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia
Central Clinical School, Monash University, Melbourne, Victoria, Australia
Baker Department of Cardiometabolic Health, The University of Melbourne, Melbourne, Australia

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Christine Yang Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia

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Yingying Liu Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia

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Anna C Calkin Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia
Central Clinical School, Monash University, Melbourne, Victoria, Australia
Baker Department of Cardiometabolic Health, The University of Melbourne, Melbourne, Australia

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Darren C Henstridge Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia
School of Health Sciences, University of Tasmania, Launceston, Tasmania, Australia

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Brian G Drew Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia
Central Clinical School, Monash University, Melbourne, Victoria, Australia
Baker Department of Cardiometabolic Health, The University of Melbourne, Melbourne, Australia

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the lack of robust changes in whole body metabolic read-outs, we were next interested to determine if TRIM28 depletion had caused detectable impacts on muscle mitochondrial function, and subsequently molecular read-outs of metabolism. A robust measure

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-23-0210
Volume/Issue:
Volume 259: Issue 2
Restricted access
Daniel M Kelly Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK

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T Hugh Jones Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK
Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK

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understood and there are few published papers that have investigated potential mechanisms by which testosterone increases insulin sensitivity and regulates glucose and lipid metabolism. The major insulin-responsive target tissues, such as skeletal muscle

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-12-0455
Volume/Issue:
Volume 217: Issue 3
Free access
Sara S Ellingwood Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, Kentucky, USA

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Alan Cheng Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, Kentucky, USA

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. From the glycogen storage diseases (GSDs), congenital disorders arising from mutations in enzymes controlling glycogen metabolism, we have obtained a clear picture in the cellular pathways involved. Along the way, this led to three Nobel prizes in

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-18-0120
Volume/Issue:
Volume 238: Issue 3
Free access
Jonathan M Mudry Section for Integrative Physiology, Section for Integrative Physiology, Department of Molecular Medicine and Surgery

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Julie Massart Section for Integrative Physiology, Section for Integrative Physiology, Department of Molecular Medicine and Surgery

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Ferenc L M Szekeres Section for Integrative Physiology, Section for Integrative Physiology, Department of Molecular Medicine and Surgery

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Anna Krook Section for Integrative Physiology, Section for Integrative Physiology, Department of Molecular Medicine and Surgery
Section for Integrative Physiology, Section for Integrative Physiology, Department of Molecular Medicine and Surgery

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stores ( Sosic et al . 2003 ). A role for TWIST proteins in metabolism has been proposed in adipose tissue, where TWIST1 is reported to regulate cytokine expression ( Pettersson et al . 2010 ). In adipose cells, TWIST1 silencing reduces fatty acid

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0474
Volume/Issue:
Volume 224: Issue 3
Free access