The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Fatty acid—induced inflammation and insulin resistance in skeletal muscle and liver
Abstract
Plasma free fatty acid (FFA) levels are elevated in obesity. FFA, by causing insulin resistance in muscle, liver, and endothelial cells, contributes to the development of type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD). The mechanism through which FFA induces insulin resistance involves intramyocellular and intrahepatocellular accumulation of triglycerides and diacylglycerol, activation of several serine/threonine kinases, reduction in tyrosine phosphorylation of the insulin receptor substrate (IRS)-1/2, and impairment of the IRS/phosphatidylinositol 3-kinase pathway of insulin signaling. FFA also produces low-grade inflammation in skeletal muscle and liver through activation of nuclear factor-kappaB, resulting in release of several proinflammatory and proatherogenic cytokines. Thus, elevated FFA levels (due to obesity or to high-fat feeding) cause insulin resistance in skeletal muscle and liver, which contributes to the development of T2DM, and produce low-grade inflammation, which contributes to the development of atherosclerotic vascular diseases and NAFLD.
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“The actions of these stimuli serve to not only further induce tissue expression and secretion of IL-6 and TNFα (via the NFκB pathway, [3, 4]), but impair control of numerous signalling pathways regulating skeletal muscle insulin signalling, glucose uptake, mitochondrial fuel oxidation and respiration that impact negatively upon skeletal muscle energy homeostasis [2, 5–7].”
From Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading (2019) · cites this paper as [5]
Citations
Cites
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Role of Mitochondrial Dysfunction in Insulin Resistance
Kim, J.-A., Wei, Y., & Sowers, J. R. (2008) · Circulation Research · doi:10.1161/circresaha.107.165472 · Cited by 1,103
Cusi, K. J. (2012) · Gastroenterology · doi:10.1053/j.gastro.2012.02.003 · Cited by 940
The Perfect Storm: Obesity, Adipocyte Dysfunction, and Metabolic Consequences
de Ferranti, S. D., & Mozaffarian, D. (2008) · Clinical Chemistry · doi:10.1373/clinchem.2007.100156 · Cited by 755
Quehenberger, O., & Dennis, E. A. (2011) · New England Journal of Medicine · doi:10.1056/nejmra1104901 · Cited by 470
Glucagon-like peptide 1 decreases lipotoxicity in non-alcoholic steatohepatitis
Armstrong, M. J., Hull, D., Guo, K., Barton, D., Hazlehurst, J. M., Gathercole, L. L., Nasiri, M., Yu, J., Gough, S. C., Newsome, P. N., et al. (2016) · Journal of Hepatology · doi:10.1016/j.jhep.2015.08.038 · Cited by 456
Metadata
- Authors
- Boden, G.
- Affiliations
- Temple University Hospital (US)
- Corresponding author
- Boden, Guenther
- Venue
- Current Diabetes Reports
- Published
- 2006-05
- Volume
- 6
- Issue
- 3
- Pages
- 177-181
- ISSN
- 1534-4827 (ISSN-L)
- 1539-0829
- OpenAlex
- W2162614886
- Cited by
- 276
- References
- 42
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 15 · 2023: 9 · 2022: 12 · 2021: 15 · 2020: 14 · 2019: 11 · 2018: 14 · 2017: 9 · 2016: 8 · 2015: 25 · 2014: 14 · 2013: 18 · 2012: 20
- FWCI
- 11.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Diabetes Reports (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01 HL 733267)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058895)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Keywords
- free fatty acids, insulin resistance, low-grade inflammation, skeletal muscle, liver, type 2 diabetes, non-alcoholic fatty liver disease, obesity, high-fat feeding, diacylglycerol, triglyceride accumulation, insulin receptor substrate, phosphatidylinositol 3-kinase, NF-κB, inflammatory cytokines, atherosclerosis
- MeSH terms
- Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Humans, Inflammation, Insulin Resistance, Liver, Obesity, Muscle, Skeletal
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