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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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Eye on the Enigmatic Link: Dysbiotic Oral Pathogens in Ocular Diseases; The Flip Side
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“…rivastigmine, and galantamine, which are drugs used to treat Alzheimer’s disease by inhibiting the activity of acetylcholinesterase, can suppress inflammation (Wu and Ballantyne 2017) and oxidative stress (Hurrle and Hsu 2017), which are risk factors for skeletal muscle insulin resistance.”
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“Under normal conditions, skeletal muscles are responsible for the majority of insulinstimulated whole-body glucose disposal; thus, the dysregulation of skeletal muscle metabolism can strongly influence whole-body glucose homeostasis and insulin sensitivity (Wu & Ballantyne, 2017).”
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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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