A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation.

By C. Erridge, T. Attinà, C. Spickett, D. Webb. American Journal of Clinical Nutrition, 2007

745 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b806222ae359e8143e60eb597792c5f78d6d253b

How researchers see this paper

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

In Epidemiology

In Immunology

Citations in the corpus

Dietary lipids, gut microbiota and lipid metabolism (2019, background): “However, weight gain, high-fat diet [88] and increased exposure of fatty acids [89, 90] may disrupt the gut barrier function allowing translocation of LPS [91, 92].”
Human Intestinal Barrier Function in Health and Disease (2016, background): “Erridge et al.96 demonstrated in a study with healthy human subjects (n=12) that a high-fat meal induced metabolic endotoxemia, which fluctuated rapidly to concentrations sufficient to induce a significant degree of inflammation.”
Dietary factors and low-grade inflammation in relation to overweight and obesity (2011, positive): “Related to this effect, the absorptive process may allow translocation of LPS from gut bacteria into the systemic circulation((168)).”
The role of the gut microbiota in energy metabolism and metabolic disease. (2009, background): “In this study, the authors found that a high-fat meal induces a metabolic endotoxemia which fluctuates rapidly in healthy subjects, from a very low concentration at baseline (between 1 to 9 pg/mL) to concentrations that may be sufficient to induce some degree of cellular activation in in vitro exper”
Effects of Gut Microbes on Nutrient Absorption and Energy Regulation (2012, background): “Consumption of a high-fat meal in both animals and humans results in both changes to the gut microbiota composition, as previously described, and significant increases in endotoxin concentrations.(104,105) It has been suggested that the increases in systemic endotoxin levels may result from increase”
Interactions between gut microbiota and host metabolism predisposing to obesity and diabetes. (2011, background): “Postprandial plasma endotoxin levels following a high-fat meal were sufficient to activate cultured human aortic endothelial cells through the release of soluble TNF-α from monocytes (81).”