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Cited by 248

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.

TLR4 and Insulin Resistance

Open access
Kim, Jane J., Sears, Dorothy D.·2010·Gastroenterology Research and Practice

Abstract

Chronic inflammation is a key feature of insulin resistance and obesity. Toll-Like Receptor 4 (TLR4), involved in modulating innate immunity, is an important mediator of insulin resistance and its comorbidities. TLR4 contributes to the development of insulin resistance and inflammation through its activation by elevated exogenous ligands (e.g., dietary fatty acids and enteric lipopolysaccharide) and endogenous ligands (e.g., free fatty acids) which are elevated in obese states. TLR4, expressed in insulin target tissues, activates proinflammatory kinases JNK, IKK, and p38 that impair insulin signal transduction directly through inhibitory phosphorylation of insulin receptor substrate (IRS) on serine residues. TLR4 activation also leads to increased transcription of pro-inflammatory genes, resulting in elevation of cytokine, chemokine, reactive oxygen species, and eicosanoid levels that promote further insulin-desensitization within the target cell itself and in other cells via paracrine and systemic effects. Increased understanding of cell type-specific TLR4-mediated effects on insulin action present the opportunity and challenge of developing related therapeutic approaches for improving insulin sensitivity while preserving innate immunity.

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Metadata

Authors
Kim, J. J., & Sears, D. D.
Venue
Gastroenterology Research and Practice
Publisher
Wiley
Published
2010
Volume
2010
Pages
1-11
ISSN
  • 1687-6121 (ISSN-L)
  • 1687-630X
OpenAlex
W2142995099
Cited by
248
References
36
FWCI
6.50
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: TLR4 and Insulin Resistance. https://app.cochat.ai/papers/10.1155/2010/212563
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Kim, J. J., & Sears, D. D. (2010). TLR4 and Insulin Resistance. Gastroenterology Research and Practice. https://doi.org/10.1155/2010/212563

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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