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Cristina Velasco Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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Marta Librán-Pérez Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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Cristina Otero-Rodiño Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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Marcos A López-Patiño Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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Jesús M Míguez Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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José Miguel Cerdá-Reverter Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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José L Soengas Laboratorio de Fisioloxía Animal, Departamento de Fisiología de Peces y Biotecnología, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, 36310 Vigo, Spain

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) through several mechanisms such as i) fatty acid metabolism by means of inhibition of carnitine palmitoyltransferase 1 (CPT1) to import fatty acid-CoA into the mitochondria for oxidation; ii) binding to fatty acid translocase (FAT/CD36), and further

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Sarah L Armour Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark

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Jade E Stanley Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA

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James Cantley Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, UK

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E Danielle Dean Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
Division of Diabetes, Endocrinology, & Metabolism, Vanderbilt University Medical Center School of Medicine, Nashville, Tennessee, USA

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Jakob G Knudsen Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark

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( Sugden et al. 2001 ) as well as other tissues ( Pilegaard et al. 2003 , Wu et al. 1998 ) and plays a crucial role in the switch between glucose and fatty acid oxidation ( Hue & Taegtmeyer 2009 ). The high expression of PDK4 suggests that a limited

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Xiaofeng Wang Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2R3

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Catherine B Chan Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2R3

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PPARγ ( Braissant et al . 1996 ). PPARα mainly regulates genes involved in fatty acid oxidation ( Kersten et al . 1999 ), while PPARγ modulate genes involved in lipogenesis, insulin signaling, and inflammation ( Mueller et al . 2002 ). Pancreatic β

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

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

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availability of substrates for mitochondrial oxidation (from glucose, amino acids and fatty acids). The consequences of failure of these adaptive responses are clearly demonstrated in the syndrome of adrenal insufficiency (in Addison's disease or

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M Kurtz Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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E Capobianco Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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V Careaga Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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N Martinez Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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M B Mazzucco Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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M Maier Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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A Jawerbaum Laboratory of Reproduction and Metabolism, UMYMFOR (CONICET‐UBA), CEFyBO‐CONICET, School of Medicine and

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fetuses and maternal diets supplemented with 6% olive oil or 6% safflower oil (enriched in unsaturated fatty acids that activate the three PPAR isotypes) prevent overproduction of nitric oxide, an excess involved in the induction of a proinflammatory

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Ricardo Rodríguez-Calvo Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Reus, Spain

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Josefa Girona Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Reus, Spain

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Josep M Alegret Department of Cardiology, Cardiovascular Research Group, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Reus, Spain

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Alba Bosquet Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Reus, Spain

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Daiana Ibarretxe Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Reus, Spain

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Lluís Masana Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Reus, Spain

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. 2013 , Liu et al . 2013 ). Among these adipokines, fatty acid-binding protein 4 (FABP4) has recently been linked to cardiovascular and metabolic diseases. Additionally, FABP4 is highly expressed in macrophages, contributing to the development of

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Nele Friedrich Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald, Ferdinand-Sauerbruch-Strasse, D-17475 Greifswald, Germany

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metabolites involved in lipid metabolism ( Kim et al . 2011 ). In liver and skeletal muscle tissue, a high-fructose diet leads to oxidative stress, elevated levels of amino acids and alterations in fatty acid biosynthesis, whereas this type of diet is related

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Eleftheria Diakogiannaki Peninsula Medical School, Institute of Biomedical and Clinical Science, John Bull Building, Plymouth PL6 8BU, UK

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Hannah J Welters Peninsula Medical School, Institute of Biomedical and Clinical Science, John Bull Building, Plymouth PL6 8BU, UK

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Noel G Morgan Peninsula Medical School, Institute of Biomedical and Clinical Science, John Bull Building, Plymouth PL6 8BU, UK

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Naassan A Allister EM Tang C Park E Uchino H Lewis GF Fantus IG Rozakis-Adcock M 2007 Free fatty acid-induced reduction in glucose-stimulated insulin secretion: evidence for a role of oxidative stress in vitro and in vivo . Diabetes 56

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Jordan S F Chan Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Tanin Shafaati Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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John R Ussher Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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general, ~90% of the ATP generated in the heart can be attributed to oxidative phosphorylation, with the remaining 10% coming from anaerobic glycolysis ( Lopaschuk et al. 2010 , Ussher et al. 2016 ). The oxidation of glucose and fatty acids represent

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Nigel Turner Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Gregory J Cooney Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Edward W Kraegen Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Clinton R Bruce Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2 . Science 291 2613 – 2616 . ( doi:10.1126/science.1056843 ) Abu-Elheiga L Oh W Kordari P Wakil SJ 2003 Acetyl-CoA carboxylase 2 mutant mice are protected against

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