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Fausto Bogazzi
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Francesco Raggi
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Federica Ultimieri
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Dania Russo
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Aldo D'Alessio Department of Endocrinology and Metabolism, Department of Chemistry and Industrial Chemistry, University of Pisa, Ospedale Cisanello, Via Paradisa 2, 56124 Pisa, Italy

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Antonella Manariti Department of Endocrinology and Metabolism, Department of Chemistry and Industrial Chemistry, University of Pisa, Ospedale Cisanello, Via Paradisa 2, 56124 Pisa, Italy

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Sandra Brogioni
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Luca Manetti
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Enio Martino
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different energy requirements. Energy metabolism in normal hearts depends on ATP production from mitochondrial oxidation of glucose and fatty acids (FA; Taegtmeyer 1994 , Stanley & Chandler 2002 ). FA oxidation is the main cardiac energy source accounting

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0194
Volume/Issue:
Volume 201: Issue 3
Free access
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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, for example, with re-feeding during recovery from stress, glucocorticoids may promote glycogen re-accumulation. The effects of glucocorticoids on fatty acid metabolism are less well understood than those on glucose metabolism and have not been reviewed

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0054
Volume/Issue:
Volume 197: Issue 2
Free access
Rengasamy Palanivel Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3

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Vivian Vu Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3

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Min Park Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3

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Xiangping Fang Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3

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Gary Sweeney Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3

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contractile performance is derived from fatty acids while the remainder (∼30%) is principally obtained via metabolism of glucose ( Stanley et al . 2005 , An & Rodrigues 2006 ). Well-controlled fatty acid metabolism is also important to prevent triglyceride

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0336
Volume/Issue:
Volume 199: Issue 3
Free access
Karen R Kelly Departments of Kinesiology and Biological Sciences, Biological Sciences, Physiology and Biophysics, College of Letters, Arts, and Sciences, University of Southern California, 3560 Watt Way, PED 107,  Los Angeles, California 90089-0652, USA Departments of

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Chin K Sung Departments of Kinesiology and Biological Sciences, Biological Sciences, Physiology and Biophysics, College of Letters, Arts, and Sciences, University of Southern California, 3560 Watt Way, PED 107,  Los Angeles, California 90089-0652, USA Departments of

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Marcia J Abbott Departments of Kinesiology and Biological Sciences, Biological Sciences, Physiology and Biophysics, College of Letters, Arts, and Sciences, University of Southern California, 3560 Watt Way, PED 107,  Los Angeles, California 90089-0652, USA Departments of

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Lorraine P Turcotte Departments of Kinesiology and Biological Sciences, Biological Sciences, Physiology and Biophysics, College of Letters, Arts, and Sciences, University of Southern California, 3560 Watt Way, PED 107,  Los Angeles, California 90089-0652, USA Departments of
Departments of Kinesiology and Biological Sciences, Biological Sciences, Physiology and Biophysics, College of Letters, Arts, and Sciences, University of Southern California, 3560 Watt Way, PED 107,  Los Angeles, California 90089-0652, USA Departments of

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LCFA transporter, fatty acid translocase (FAT/CD36), from an intracellular compartment to the PM ( Dyck et al . 2001 , Luiken et al . 2002 ). However, the effects of insulin on muscle LCFA metabolism, independent of its stimulatory effects on glucose

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0122
Volume/Issue:
Volume 198: Issue 2
Free access
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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JF Luiken JJ Bonen A 2010 Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease . Physiological Reviews 90 367 – 417 . ( doi:10.1152/physrev.00003.2009 ) Goodpaster BH He J Watkins S Kelley DE 2001

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0397
Volume/Issue:
Volume 220: Issue 2
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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-inositol states could impact placental lipid metabolism with consequences for fetal development. In this study we sought to address the specific hypothesis that myo-inositol treatment alters the processing of fatty acids in normal human term placenta. We

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0267
Volume/Issue:
Volume 243: Issue 1
Free access
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

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0391
Volume/Issue:
Volume 228: Issue 1
Free access
A Margot Umpleby Diabetes and Metabolic Medicine, Faculty of Health and Metabolic Sciences, University of Surrey, Leggett Building, Daphne Jackson Road, Manor Park, Guildford GU2 7WG, UK

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mellitus and atherosclerotic cardiovascular disease ( Hubert et al . 1983 , de Marco et al . 1999 ). Fatty acids are one of the mediators of insulin resistance ( Boden 1998 ), and an imbalance in fatty acid metabolism results in the accumulation of

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0610
Volume/Issue:
Volume 226: Issue 3
Free access
Eleftheria Diakogiannaki Peninsula Medical School, Institute of Biomedical and Clinical Sciences, John Bull Building, Plymouth, Devon PL6 8BU, UK
School of Medicine, Institute of Human Nutrition, University of Southampton, Southampton SO16 7PX, UK

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Shalinee Dhayal Peninsula Medical School, Institute of Biomedical and Clinical Sciences, John Bull Building, Plymouth, Devon PL6 8BU, UK
School of Medicine, Institute of Human Nutrition, University of Southampton, Southampton SO16 7PX, UK

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Caroline E Childs Peninsula Medical School, Institute of Biomedical and Clinical Sciences, John Bull Building, Plymouth, Devon PL6 8BU, UK
School of Medicine, Institute of Human Nutrition, University of Southampton, Southampton SO16 7PX, UK

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Philip C Calder Peninsula Medical School, Institute of Biomedical and Clinical Sciences, John Bull Building, Plymouth, Devon PL6 8BU, UK
School of Medicine, Institute of Human Nutrition, University of Southampton, Southampton SO16 7PX, UK

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Hannah J Welters Peninsula Medical School, Institute of Biomedical and Clinical Sciences, John Bull Building, Plymouth, Devon PL6 8BU, UK
School of Medicine, Institute of Human Nutrition, University of Southampton, Southampton SO16 7PX, UK

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Noel G Morgan Peninsula Medical School, Institute of Biomedical and Clinical Sciences, John Bull Building, Plymouth, Devon PL6 8BU, UK
School of Medicine, Institute of Human Nutrition, University of Southampton, Southampton SO16 7PX, UK

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then available for metabolism by β-oxidation. Inhibition of CPT-1 therefore increases the availability of fatty acids in the cytosol, leading to their diversion away from oxidative metabolism and towards TAG formation. Accordingly, cells exposed to

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0082
Volume/Issue:
Volume 194: Issue 2
Free access
Hannah M Eggink Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands

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Lauren L Tambyrajah Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Rosa van den Berg Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Isabel M Mol Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Jose K van den Heuvel Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Martijn Koehorst Department of Pediatrics and Laboratory Medicine, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands

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Albert K Groen Department of Pediatrics and Laboratory Medicine, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
Department of Vascular Medicine, Amsterdam Diabetes Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Anita Boelen Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Andries Kalsbeek Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands

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Johannes A Romijn Department of Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Patrick C N Rensen Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Sander Kooijman Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Maarten R Soeters Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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-described effects of BAs in lipid and carbohydrate metabolism, we hypothesized that central effects of BA contribute to the regulation of energy metabolism. Therefore, the aim of the present study was to determine the effects of central bile acid signaling on

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0503
Volume/Issue:
Volume 236: Issue 2
Free access