Metabolic Endotoxemia Initiates Obesity and Insulin Resistance

By Patrice D Cani, J. Amar, M. Iglesias, M. Poggi, C. Knauf, D. Bastelica, A. Neyrinck, F. Fava, K. Tuohy, C. Chabo and 12 more. Diabetes, 2007

6,138 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/0b230b85885acfd2d947357c18763387e3ebb40b

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Citations in the corpus

Negative Effects of a High-Fat Diet on Intestinal Permeability: A Review. (2019, background): “(91) was the first to demonstrate that serum LPS levels varied in the fast compared with the fed state and that an HFD was responsible for 3-fold greater serum LPS in mice.”
Intestinal microbiota in patients with nonalcoholic fatty liver disease (2013, neutral): “Insulin (pmol/L) 21 (15-61) 33 (15-465) 97 (29-437)”
The Intestinal Microbiome in Early Life: Health and Disease (2014, background): “The mechanisms that the microbiota use to signal a shift in host metabolism include signaling through TLR5 (195), glucagon-like peptide (GLP)-1/2 (196), and mediating systemic LPS levels (197).”
Germ-free C57BL/6J mice are resistant to high-fat-diet-induced insulin resistance and have altered cholesterol metabolism. (2010, background): “Alternatively, many groups, including our own, have suggested that lipopolysaccharides (LPS) absorbed from gram-negative bacteria residing in the intestine may induce insulin resistance in the host (7, 8, 19).”
Gut microbiome and health: mechanistic insights (2022, background): “This is the case in metabolic endotoxaemia, in which high-fat diet and weight gain have been associated with a higher gut permeability and subsequent systemic (mild) elevation in circulating plasma LPS. 100 This causes a state of low-grade inflammation, which is a pathological feature of a range of ”
Regulation of Inflammation by Short Chain Fatty Acids (2011, background): “Some of the compounds that have been implicated in the effects of microbiota on host cells are microbial-derived ligands of toll like receptors (TLRs) such as LPS and flagellin, which activate, respectively, TLR-4 and -5 and modulate distinct aspects of host metabolism and immune responses [3,7].”