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Nan Yang Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Giorgio Caratti Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Louise M Ince Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Toryn M Poolman Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Peter J Trebble Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Cathy M Holt Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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David W Ray Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Laura C Matthews Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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signalling; therefore, there is great interest in defining mechanisms underlying how local tissue Gc sensitivity is being regulated ( Yang et al . 2012 ). Amongst the best-characterised alterations in local Gc sensitivity is the acquired resistance that

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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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C Tanaka T Noguchi M Tomita T Fujikura J Yamamoto Y 2010 Glucocorticoid reamplification within cells intensifies NF-κB and MAPK signaling and reinforces inflammation in activated preadipocytes . American Journal of Physiology

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Hyo Youl Moon
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Parkyong Song BioSignal Network Laboratory, Division of Molecular and Life Sciences, Lee Gil Ya Cancer and Diabetes Institute, School of Nano-Biotechnology and Chemical Engineering, Ulsan National Institute of Science and Technology, Engineering Building 104, 689-805 Ulsan, Republic of Korea

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Cheol Soo Choi BioSignal Network Laboratory, Division of Molecular and Life Sciences, Lee Gil Ya Cancer and Diabetes Institute, School of Nano-Biotechnology and Chemical Engineering, Ulsan National Institute of Science and Technology, Engineering Building 104, 689-805 Ulsan, Republic of Korea

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Sung Ho Ryu BioSignal Network Laboratory, Division of Molecular and Life Sciences, Lee Gil Ya Cancer and Diabetes Institute, School of Nano-Biotechnology and Chemical Engineering, Ulsan National Institute of Science and Technology, Engineering Building 104, 689-805 Ulsan, Republic of Korea

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Pann-Ghill Suh
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activation of the ERK MAPK signalling pathway by macrophage migration inhibitory factor (MIF) and dependence on JAB1/CSN5 and Src kinase activity . Cell Signalling 18 688 – 703 . ( doi:10.1016/j.cellsig.2005.06.013 ) McGarry JD Brown NF 1997 The

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Antonia Hufnagel University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Level 4, Addenbrooke’s Hospital, Cambridge, Cambridgeshire, UK

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Laura Dearden University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Level 4, Addenbrooke’s Hospital, Cambridge, Cambridgeshire, UK

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Denise S Fernandez-Twinn University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Level 4, Addenbrooke’s Hospital, Cambridge, Cambridgeshire, UK

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Susan E Ozanne University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Level 4, Addenbrooke’s Hospital, Cambridge, Cambridgeshire, UK

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in pregnancy are summarised. In obese women, impaired insulin signalling and/or pancreatic ß-cell dysfunction predispose to the development of GDM. Even before diagnosis of GDM, higher insulin levels can be detected early in pregnancy (week 16

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Helen L Jeanes
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Caroline Tabor
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Darcey Black Centre for Cardiovascular Science, Organon Laboratories Ltd, Department Pharmacology, University of Edinburgh, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Antwan Ederveen Centre for Cardiovascular Science, Organon Laboratories Ltd, Department Pharmacology, University of Edinburgh, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

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Gillian A Gray
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of perfusion and administration of CP-H spin trap was repeated. Finally, to determine the contribution of superoxide radicals to the oxidant signal generated by the heart 500 U superoxide dismutase (SOD) was perfused through the entire heart along

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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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responsible for this hyperoxidation of PRDX3. Inactivation of PRDX3 results in accumulation of H 2 O 2 which can diffuse into the cytosol, activating p38 MAPK signalling pathways with subsequent suppression of STAR protein synthesis and inhibition of

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Amanda E Garza Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Elijah Trefts Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Isis A Katayama Rangel Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Danielle Brooks Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Rene Baudrand Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
Department of Endocrinology, School of Medicine, Pontificia Universidad Catolica De Chile, Santiago, Chile

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Burhanuddin Moize Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Jose R Romero Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Sanjay Ranjit Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Thitinan Treesaranuwattana Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Tham M Yao Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Gail K Adler Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Luminita H Pojoga Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Gordon H Williams Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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in the mitogen-activated protein kinase (MAPK) pathway and with intracellular calcium regulation ( Funder 2017 ). It is well known that activation of the aldosterone/MR pathway, in the presence of a liberal sodium (1.6% Na + ), diet, is a risk

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Renata Risi Department of Experimental Medicine, Sapienza University of Rome, Sapienza University of Rome, Rome, Italy
University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, UK

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Antonio Vidal-Puig University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, UK
Cambridge University Nanjing Centre of Technology and Innovation, Nanjing, P. R. China
Centro de Investigacion Principe Felipe, Valencia, Spain

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Guillaume Bidault University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, UK

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secretion, which suggests they might be initial signals communicating the need for increased insulin secretion to blunt lipolysis. These observations highlight the dual role of FAs in regulating β-cell function and the necessity to maintain appropriate lipid

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Esther Nuñez-Durán Department of Molecular and Clinical Medicine, Lundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden

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Belén Chanclón Department of Molecular and Clinical Medicine, Lundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden
Department of Metabolic Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden

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Silva Sütt Department of Molecular and Clinical Medicine, Lundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden

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Joana Real Department of Metabolic Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden

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Hanns-Ulrich Marschall Department of Molecular and Clinical Medicine, Wallenberg Laboratory, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden

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Ingrid Wernstedt Asterholm Department of Metabolic Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden

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Emmelie Cansby Department of Molecular and Clinical Medicine, Lundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden

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Margit Mahlapuu Department of Molecular and Clinical Medicine, Lundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden

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( Supplementary Fig. 4 ). To assess mitochondrial activity, we measured the signal for MitoTracker Red, a fluorescent dye that specifically accumulates within respiring mitochondria. Surprisingly, we found that the relative area staining for MitoTracker Red was 6

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Nele Cielen Laboratory of Respiratory Diseases, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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Nele Heulens Laboratory of Respiratory Diseases, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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Karen Maes Laboratory of Respiratory Diseases, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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Geert Carmeliet Laboratory of Clinical and Experimental Endocrinology, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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Chantal Mathieu Laboratory of Clinical and Experimental Endocrinology, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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Wim Janssens Laboratory of Respiratory Diseases, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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Ghislaine Gayan-Ramirez Laboratory of Respiratory Diseases, Department of Clinical and Experimental Medicine, KULeuven, Leuven, Belgium

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period of time, and then slowly expires the animal to residual volume ( De Vleeschauwer et al. 2011 , Rinaldi et al. 2012 ). Lung compliance is calculated from the pressure–volume curve, and an average of three signals was used for subsequent

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