Endotoxemia of metabolic syndrome: a pivotal mediator of meta-inflammation

Metab Syndr Relat Disord. 2014 Nov;12(9):454-6. doi: 10.1089/met.2014.1504. Epub 2014 Aug 27.


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.

Publication types

  • Review

MeSH terms

  • Digestive System / microbiology
  • Digestive System / physiopathology
  • Endotoxemia / complications*
  • Endotoxins / blood
  • Humans
  • Inflammation / etiology*
  • Insulin Resistance
  • Metabolic Syndrome / complications*
  • Metabolic Syndrome / therapy
  • Microbiota
  • Permeability


  • Endotoxins