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Skeletal muscle inflammation and insulin resistance in obesity
Open accessAbstract
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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“The IKK/NF-kB pathway is activated by TNF-α, IL-1β, and free-fatty acids [62].”
From Sarcopenic obesity, insulin resistance, and their implications in cardiovascular and metabolic consequences (2020) · cites this paper as [62]
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“Besides, skeletal muscle can strongly influence whole-body glucose homeostasis and insulin sensitivity (Wu and Ballantyne, 2017).”
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“This combination of lipid intermediaries and inflammatory signals stimulates serine kinases such as phospho-C-JUN-N-terminal kinase (p-JNK), IkB kinase (IKK), and protein kinase C θ (PKC θ), leading to insulin resistance (Glass and Olefsky, 2012; Wu and Ballantyne, 2017).”
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Background
Metadata
- Authors
- Wu, H., & Ballantyne, C. M.
- Affiliations
- Houston Methodist (US)
- Corresponding author
- Ballantyne, Christie M.
- Venue
- Journal of Clinical Investigation
- Published
- 2017-01-03
- Volume
- 127
- Issue
- 1
- Pages
- 43-54
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5199705
- OpenAlex
- W2561422649
- Cited by
- 695
- References
- 171
- Citations by year
- 2026: 66 · 2025: 92 · 2024: 103 · 2023: 84 · 2022: 98 · 2021: 95 · 2020: 76 · 2019: 45 · 2018: 29 · 2017: 7
- FWCI
- 5.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association (AHA16GRNT30410012)
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL098839)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK078847)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- skeletal muscle inflammation, insulin resistance, obesity, type 2 diabetes, chronic inflammation, immune cell infiltration, proinflammatory molecules, paracrine signaling, visceral adipose tissue, glucose homeostasis
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Glucose, Humans, Inflammation, Insulin Resistance, Myositis, Obesity, Muscle, Skeletal, Muscle Fibers, Skeletal, Intra-Abdominal Fat
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