Loss-of-Function Mutation in Toll-Like Receptor 4 Prevents Diet-Induced Obesity and Insulin Resistance

By D. Tsukumo, M. A. Carvalho-Filho, J. Carvalheira, P. Prada, S. Hirabara, A. Schenka, E. Araújo, J. Vassallo, R. Curi, L. Velloso and 1 more. Diabetes, 2007

835 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/2b4a548101328228433b4e0a8a4feec07d4488ac

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Patrice D Cani
2. N. Delzenne
3. Herbert Tilg
4. A. Moschen
5. A. Chawla
6. Ebru Erbay
7. A. Neyrinck
8. S. Summers

In Immunology

1. A. Chawla
2. Y. Goh
3. Yuanqing Liu
4. S. Summers
5. Patrice D Cani
6. K. Nguyen
7. Ebru Erbay
8. Céline Vaure

Citations in the corpus

• Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice (2008, background): “We and others have recently demonstrated that the mechanisms of highfat diet-induced inflammation and metabolic disorders were clearly linked to LPS (4;24-28).”
• A ceramide-centric view of insulin resistance. (2012, background): “One mechanism for this involves the activation of toll-like receptors (TLRs), which induce the transcription of inflammatory cytokines such as TNFa and interleukin-6 (IL6), by saturated fats (Senn, 2006; Shi et al., 2006; Tsukumo et al., 2007).”
• Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes (2008, background): “A loss-of-function point mutation in TLR4 prevents diet-induced obesity and insulin resistance in mice fed on a high-fat diet, as well as saturated fatty acid-induced insulin resistance in isolated muscle from those mic”
• A Comparative Review of Toll-Like Receptor 4 Expression and Functionality in Different Animal Species (2014, background): “Fibronectin type III extra domain A (26, 27) and saturated fatty acids (28, 29) are potentially recognized by human and mouse TLR4, and heme by mouse TLR4 (30).”
• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “TLR-4–deficient mice are protected from high-fat diet-induced inflammation and insulin resistance.(50) It is, however, not universally accepted whether saturated free fatty acids are ligands for certain TLRs because it has been demonstrated that saturated fatty acids might not directly stimulate TLR”