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Kok Lim Kua Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Shanming Hu Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Chunlin Wang Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Jianrong Yao Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Diana Dang Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Alexander B Sawatzke Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Jeffrey L Segar Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Kai Wang Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA

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Andrew W Norris Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA
Department of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA
Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, Iowa, USA

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hyperglycemia rapidly developed skeletal muscle insulin resistance while still in utero . The insulin signaling defects persisted through postnatal life, localized to skeletal muscle. Uteroplacental insufficiency and fetal hyperinsulinism did not have these

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Sergio Di Meo Dipartimento di Biologia, Università di Napoli ‘Federico II’, Napoli, Italy

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Susanna Iossa Dipartimento di Biologia, Università di Napoli ‘Federico II’, Napoli, Italy

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Paola Venditti Dipartimento di Biologia, Università di Napoli ‘Federico II’, Napoli, Italy

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development. Exercise and insulin resistance It is known that regular exercise elicit adaptive responses that improves the metabolism of glucose and lipids in skeletal muscles during the resting state. Moreover, it is well established that health

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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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(obesity) and reduced insulin action (insulin resistance) in muscle, this article will deal with FAs as an alternative energy substrate to glucose, the relevance of this substrate competition to overall energy expenditure and an assessment of the various

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Brenna Osborne Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
Department of Pharmacology, School of Biomedical Sciences, UNSW Sydney, New South Wales, Australia
Department of Cellular and Molecular Medicine, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Lauren E Wright Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia

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Amanda E Brandon Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
Charles Perkins Centre, University of Sydney, New South Wales, Australia

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Ella Stuart Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia

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Lewin Small Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia

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Joris Hoeks NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands

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Patrick Schrauwen NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands

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David A Sinclair Department of Genetics, Paul F. Glenn Center for Biology of Aging Research, Harvard Medical School, Boston, Massachusetts, USA

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Magdalene K Montgomery Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
Department of Anatomy & Physiology, School of Biomedical Sciences, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Victoria, Australia

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Gregory J Cooney Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
Charles Perkins Centre, University of Sydney, New South Wales, Australia

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Nigel Turner Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
Department of Pharmacology, School of Biomedical Sciences, UNSW Sydney, New South Wales, Australia
Cellular Bioenergetics Laboratory, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia

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Introduction Mitochondrial dysfunction has been associated with skeletal muscle insulin resistance and type 2 diabetes in humans as well as in animal models of lipid-induced insulin resistance (reviewed in Montgomery & Turner 2015 ). SIRT3 is

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Meng Guo School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Yuna Li School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Yan Wang School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Zhenkun Li School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Xiaohong Li School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Peikun Zhao School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Changlong Li School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Jianyi Lv School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Xin Liu School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Xiaoyan Du School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Zhenwen Chen School of Basic Medical Sciences, Capital Medical University, Beijing Key Laboratory of Cancer Invasion & Metastasis Research, Beijing, People’s Republic of China

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Introduction As a major metabolic tissue, skeletal muscle constitutes 40% of the total body mass and plays a predominant role in postprandial glucose disposal in humans ( DeFronzo et al. 1981 ). Insulin resistance in skeletal muscle is an

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Sergio Di Meo Department of Biology, University of Naples ‘Federico II’, Naples, Italy

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Susanna Iossa Department of Biology, University of Naples ‘Federico II’, Naples, Italy

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Paola Venditti Department of Biology, University of Naples ‘Federico II’, Naples, Italy

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. Adiponectin is believed to activate the 5′-AMP activated protein kinase (AMPK), which seems to play a role in insulin-independent glucose uptake by the muscle ( Yamauchi et al . 2002 ). Insulin resistance IR is a reduction of the responses of

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Sattar Gorgani-Firuzjaee Department of Biochemistry, Department of Clinical Biochemistry, Endocrinology and Metabolism Research Centre, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran

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Salar Bakhtiyari Department of Biochemistry, Department of Clinical Biochemistry, Endocrinology and Metabolism Research Centre, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran

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Abolfazl Golestani Department of Biochemistry, Department of Clinical Biochemistry, Endocrinology and Metabolism Research Centre, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran

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Reza Meshkani Department of Biochemistry, Department of Clinical Biochemistry, Endocrinology and Metabolism Research Centre, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran
Department of Biochemistry, Department of Clinical Biochemistry, Endocrinology and Metabolism Research Centre, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran

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Introduction Insulin resistance plays a major role in the development of some diseases such as type 2 diabetes (T2D) and metabolic syndrome ( Czech 2002 ). Resistance to the cellular actions of insulin causes reduced glucose uptake in muscle

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Maristela Mitiko Okamoto
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Gabriel Forato Anhê Department of Physiology and Biophysics, Department of Pharmacology, Diabetes Unit, Institute of Biomedical Sciences, University of São Paulo, Avenida Prof. Lineu Prestes, 1524, 05505-900 São Paulo (SP), Brazil

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Robinson Sabino-Silva
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Milano Felipe dos Santos Ferreira Marques
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Helayne Soares Freitas
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Rosana Cristina Tieko Mori
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Karla Fabiana S Melo Department of Physiology and Biophysics, Department of Pharmacology, Diabetes Unit, Institute of Biomedical Sciences, University of São Paulo, Avenida Prof. Lineu Prestes, 1524, 05505-900 São Paulo (SP), Brazil

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Ubiratan Fabres Machado
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insulinopenic and well-treated hyperinsulinemic subjects. Insulin resistance in insulinopenic diabetic rats has been associated with impaired glucose disposal in liver and skeletal muscle, similar to T2DM ( Camps et al . 1992 , Kainulainen et al . 1994

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Camilla Alexanderson
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Elias Eriksson Department of Physiology, Department of Pharmacology, Wallenberg Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Göteborg University, Box 434, SE-405 30 Göteborg, Sweden

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Elisabet Stener-Victorin
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Malin Lönn Department of Physiology, Department of Pharmacology, Wallenberg Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Göteborg University, Box 434, SE-405 30 Göteborg, Sweden

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Agneta Holmäng
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resistance ( DeFronzo 1992 ). Although adipose tissue accounts for only a small portion of glucose disposal ( DeFronzo 1992 ), it produces adipokines, which serve as endocrine mediators and influence the development of insulin resistance in skeletal muscle

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Richard R Almon
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Debra C DuBois
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Jin Y Jin
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William J Jusko
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increased gluconeogenesis in the liver and kidney, net muscle-protein breakdown to provide gluconeogenic substrates, insulin resistance of peripheral tissues including skeletal muscle, and lipid mobilization. Glucocorticoids also suppress

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