TLR4 links innate immunity and fatty acid-induced insulin resistance.

By Hang Shi, M. Kokoeva, Karen E. Inouye, Iphigenia Tzameli, Huali Yin, J. Flier. Journal of Clinical Investigation, 2006

3,637 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/fca1391962ca031812a62d692b46dbf581f03972

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Citations in the corpus

INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, positive): “Furthermore, Tlr4 knockout (KO) mice are resistant to the effects of high-fat diets to cause decreased insulin sensitivity (Saberi et al., 2009; Shi et al., 2006) (Figure 1).”
Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes (2008, background): “It has been suggested that FFAs function through TLR4 on adipose cells and macrophages to induce inflammatory signalling and suppress insulin signallin”
Human nutrition, the gut microbiome, and immune system: envisioning the future (2011, background): “Furthermore, nutrients are known to activate inflammatory arms of the immune system directl”
Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “The fact that M1 and MMe macrophages differed markedly in surface marker expression was surprising given that palmitate is thought to mimic LPS action by binding to TLRs (Himes and Smith, 2010; Shi et al., 2006).”
Intestinal mucosal adherence and translocation of commensal bacteria at the early onset of type 2 diabetes: molecular mechanisms and probiotic treatment (2011, neutral): “A dramatic changein dietary habits, characterized by an increased intake of lipids, has been suggested to be mainly responsible for the dramatic rise in metabolic diseasesthrough mechanisms, whichinducelowgrade inﬂammation (Hotamisligil, 2006; Shi et al, 2006; Shoelson et al, 2006).”
Inflammatory mechanisms linking obesity and metabolic disease (2017, background): “As mentioned above, PRRs that sense endogenous ligands induced under obesogenic conditions may also play a key role, as TLR4-deficient mice are protected from the inflammatory activation induced by obesity (15).”
Effect of Probiotic Supplementation on Cognitive Function and Metabolic Status in Alzheimer's Disease: A Randomized, Double-Blind and Controlled Trial (2016, background): “…intake may improve markers of insulin metabolism and lipid profiles by reducing cytokines and suppressing the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway (Shi et al., 2006) and gut microbiotashort chain fatty acids (SCFA)-hormone axis (Yadav et al., 2013).”
Impact of the gut microbiota on inflammation, obesity, and metabolic disease (2016, background): “In particular, growth of Bacteroidetes was stimulated in obese mice co-housed with lean mice and was associated with the increased expression of proteins involved in branchedchain amino acid catabolism and increased production of SCFAs [47].”
Sphingolipids, insulin resistance, and metabolic disease: new insights from in vivo manipulation of sphingolipid metabolism. (2008, background): “Supporting the hypothesis that TLRs are essential for promoting ceramide accrual is the observation that the subset of fatty acids that induce ceramide (13) are similar to those that activate TLRs (56, 57).”
Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice (2008, result): “These results are in line with our and other previous data showing that in the absence of metabolic endotoxemia or LPS receptor, dietary lipids are not sufficient to induce metabolic disorders (4,6,25,28).”
Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Even if NLRP3 inflammasome activation in different cell types has not been completely elucidated, several evidences demonstrated that accumulation of toxic lipids and DAMPs- and PAMPS-mediated TLR signaling activates NLRP3 inflammasome [45,163,165].”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “For example, in obesity, the epithelial layer of the gut becomes leaky, allowing microflora-derived products access to the systemic circulation, and high circulating levels of the potent TLR4 agonist lipopolysaccharide (LPS) in obese states have been well documente”