Skeletal muscle inflammation and insulin resistance in obesity
Huaizhu Wu1,2 and Christie M. Ballantyne1,3,4
1Department of Medicine,
2Department of Pediatrics, and
3Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
4Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital and Baylor College of Medicine, Houston, Texas, USA.
Address correspondence to: Huaizhu Wu or Christie M. Ballantyne, Baylor College of Medicine, 6565 Fannin, M.S. A-601, Houston, Texas 77030, USA. Phone: 713.798.4141; E-mail: hwu@bcm.edu. (H. Wu). Phone: 713.798.5034; E-mail: cmb@bcm.edu (C.M. Ballantyne).
Find articles by Wu, H. in: JCI | PubMed | Google Scholar
1Department of Medicine,
2Department of Pediatrics, and
3Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
4Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital and Baylor College of Medicine, Houston, Texas, USA.
Address correspondence to: Huaizhu Wu or Christie M. Ballantyne, Baylor College of Medicine, 6565 Fannin, M.S. A-601, Houston, Texas 77030, USA. Phone: 713.798.4141; E-mail: hwu@bcm.edu. (H. Wu). Phone: 713.798.5034; E-mail: cmb@bcm.edu (C.M. Ballantyne).
Find articles by Ballantyne, C. in: JCI | PubMed | Google Scholar
First published January 3, 2017 - More info
J Clin Invest. 2017;127(1):43–54. doi:10.1172/JCI88880.
Copyright © 2017, American Society for Clinical Investigation
Obesity is associated with chronic inflammation, which contributes to insulin resistance and type 2 diabetes mellitus. Under normal conditions, skeletal muscle is responsible for the majority of insulin-stimulated whole-body glucose disposal; thus, dysregulation of skeletal muscle metabolism can strongly influence whole-body glucose homeostasis and insulin sensitivity. Increasing evidence suggests that inflammation occurs in skeletal muscle in obesity and is mainly manifested by increased immune cell infiltration and proinflammatory activation in intermyocellular and perimuscular adipose tissue. By secreting proinflammatory molecules, immune cells may induce myocyte inflammation, adversely regulate myocyte metabolism, and contribute to insulin resistance via paracrine effects. Increased influx of fatty acids and inflammatory molecules from other tissues, particularly visceral adipose tissue, can also induce muscle inflammation and negatively regulate myocyte metabolism, leading to insulin resistance.
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