title: Endotoxemia of metabolic syndrome: a pivotal mediator of meta-inflammation.
abstract: Endotoxemia, which is now emerging as a feature of metabolic syndrome, is believed to contribute to the chronic low-grade inflammatory status and insulin resistance of the syndrome. Lipopolysaccharides (LPS), or endotoxins, bind to LPS-binding protein and activate pattern recognition receptors, classically Toll-like receptor-4, mediating inflammation. Increased gut permeability and changes in composition and diversity of gut microbiome have been proposed as possible mechanisms to explain increased circulating endotoxins in metabolic syndrome. Endotoxins are also believed to be delivered into the circulation by chylomicrons. Weight loss and probiotic and prebiotic therapeutic strategies can reduce endotoxemia, inflammation, and insulin resistance in metabolic syndrome.
authors.affiliation: Laboratory for Atherosclerosis and Metabolic Research, Department of Pathology, Division of Endocrinology, Diabetes and Metabolism, University of California Davis Medical Center , and VA Medical Center, Sacramento, California.
authors.forename: Ishwarlal
authors.initials: I
authors.lastname: Jialal
authors.forename: Uthra
authors.initials: U
authors.lastname: Rajamani
mesh_terms: D004064:Digestive System / Q000382:microbiology / Q000503:physiopathology; D019446:Endotoxemia / Q000150:complications*; D004731:Endotoxins / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D007333:Insulin Resistance; D024821:Metabolic Syndrome / Q000150:complications* / Q000628:therapy; D064307:Microbiota; D010539:Permeability
chemical_list: D004731:Endotoxins