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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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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
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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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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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
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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Charles Perkins Centre, University of Sydney, New South Wales, Australia
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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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Charles Perkins Centre, University of Sydney, New South Wales, Australia
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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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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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. 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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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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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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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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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