The DOI matches its Crossref record; 170 of the 171 references it cites were found in a registry or an index.
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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1 retracted
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RetractedObesity is associated with macrophage accumulation in adipose tissue
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Inflammation and metabolic disorders
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Macrophage plasticity and polarization: in vivo veritas
Sica, A., & Mantovani, A. (2012) · Journal of Clinical Investigation · doi:10.1172/jci59643 · Cited by 6,335
A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis
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Mutation of the mouse klotho gene leads to a syndrome resembling ageing
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Mechanisms of fatty acid-induced inhibition of glucose uptake.
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TLR4 links innate immunity and fatty acid-induced insulin resistance
Shi, H., Kokoeva, M. V., Inouye, K., Tzameli, I., Yin, H., & Flier, J. S. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28898 · Cited by 3,690
Research works printed but not linked: 4
- 10.1172/JCI19246 · DOI · Paper page
- 10.1172/JCI19451 · DOI · Paper page
- 10.1074/jbc.M513304200 · DOI · Paper page
- 10.1172/JCI22230 · DOI · Paper page
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Pathophysiology of type 2 diabetes mellitus
Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., Ostolaza, H., & Martín, C. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21176275 · Cited by 3,360
“This ultimately leads to myocyte inflammation, impaired myocyte metabolism, and contributes to IR via paracrine effects [162].”
BackgroundInflammatory mechanisms linking obesity and metabolic disease
Saltiel, A. R., & Olefsky, J. M. (2017) · Journal of Clinical Investigation · doi:10.1172/jci92035 · Cited by 2,212
“Huaizhu Wu and Christie Ballan-tyne discuss how the mechanisms described above mediate interactions between immune cells, adipose tissue, and skeletal muscle to influence whole-body glucose homeostasis (37).”
BackgroundMetabolic Inflammation and Insulin Resistance in Obesity
Wu, H., & Ballantyne, C. M. (2020) · Circulation Research · doi:10.1161/circresaha.119.315896 · Cited by 1,059
“DOI: 10.1161/CIRCRESAHA.119.315896 May 22, 2020 1559 Anti-Inflammatory Thrombosis Outcomes Study) did not show long-term benefits in reducing HbA1c and reductions in incident T2DM.186 The potential of other therapies targeting the NLRP3 inflammasome pathway in treating T2DM remains to be assessed.”
BackgroundInfluentialSelf-citationThe Liver as an Endocrine Organ—Linking NAFLD and Insulin Resistance
Watt, M. J., Miotto, P. M., De Nardo, W., & Montgomery, M. K. (2019) · Endocrine Reviews · doi:10.1210/er.2019-00034 · Cited by 615
Short-chain fatty acids as potential regulators of skeletal muscle metabolism and function
Frampton, J. E., Murphy, K. G., Frost, G. S., & Chambers, E. S. (2020) · Nature Metabolism · doi:10.1038/s42255-020-0188-7 · Cited by 552
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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