Skeletal muscle inflammation and insulin resistance in obesity
2017/01/02 by Huaizhu Wu, Christie M. Ballantyne · 689 citations
Medicine · #Adipokines, Inflammation, and Metabolic Diseases #Adipose Tissue and Metabolism #Adipose tissue #Biology #Carbohydrate metabolism #Cardiovascular Disease and Adiposity #Endocrinology #Glucose homeostasis #Glucose uptake #Inflammation #Insulin #Insulin resistance #Internal medicine #Medicine #Myocyte #Proinflammatory cytokine #Skeletal muscle
paper · pdf · doi:10.1172/jci88880
published in Journal of Clinical Investigation 127(1), 43-54 (American Society for Clinical Investigation)
openalex publication_date 2017/01/02 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
Abstract
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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