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Title: Muscle atrophy in patients with Type 2 Diabetes Mellitus: roles of inflammatory pathways, physical activity and exercise.
Austin Authors: Perry, Ben D;Caldow, Marissa K;Brennan-Speranza, Tara C;Sbaraglia, Melissa;Jerums, George ;Garnham, Andrew;Wong, Chiew;Levinger, Pazit;Asrar Ul Haq, Muhammad;Hare, David L ;Price, S Russ;Levinger, Itamar 
Affiliation: Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Australia
Renal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA
Department of Physiology, Bosch Institute for Medical Research, University of Sydney, Sydney, Australia
University of Melbourne and the Department of Endocrinology, Austin Health, Melbourne, Australia
School of Exercise & Nutrition Sciences, Deakin University, Melbourne, Australia
The University of Melbourne, Melbourne, Victoria, Australia
Department of Cardiology, Austin Health, Heidelberg, Victoria, Australia
Atlanta Veterans Affairs Medical Centre, Decatur, Georgia, USA
Basic and Clinical Myology Laboratory, Department of Physiology, The University of Melbourne, Melbourne, Victoria, Australia
The Northern Heart, The Northern Hospital, Melbourne, Australia
Issue Date: 2016
Publication information: Exercise immunology review 2016; 22: 94-109
Abstract: Muscle atrophy is caused by an imbalance in contractile protein synthesis and degradation which can be triggered by various conditions including Type 2 Diabetes Mellitus (T2DM). Reduced muscle quality in patients with T2DM adversely affects muscle function, the capacity to perform activities of daily living, quality of life and ultimately may increase the risk of premature mortality. Systemic inflammation initiated by obesity and prolonged overnutrition not only contributes to insulin resistance typical of T2DM, but also promotes muscle atrophy via decreased muscle protein synthesis and increased ubiquitin-proteasome, lysosomal-proteasome and caspase 3- mediated protein degradation. Emerging evidence suggests that the inflammation-sensitive Nuclear Factor κ B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3) pathways may contribute to muscle atrophy in T2DM. In contrast, exercise appears to be an effective tool in promoting muscle hypertrophy, in part due to its effect on systemic and local (skeletal muscle) inflammation. The current review discusses the role inflammation plays in muscle atrophy in T2DM and the role of exercise training in minimising the effect of inflammatory markers on skeletal muscle. We also report original data from a cohort of obese patients with T2DM compared to age-matched controls and demonstrate that patients with T2DM have 60% higher skeletal muscle expression of the atrophy transcription factor FoxO1. This review concludes that inflammatory pathways in muscle, in particular, NF-κB, potentially contribute to T2DM-mediated muscle atrophy. Further in-vivo and longitudinal human research is required to better understand the role of inflammation in T2DM-mediated atrophy and the anti-inflammatory effect of exercise training under these conditions.
ORCID: 0000-0001-9554-6556
PubMed URL: 26859514
ISSN: 1077-5552
Type: Journal Article
Subjects: Skeletal muscle
Appears in Collections:Journal articles

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