Metabolic endotoxaemia: is it more than just a gut feeling?

Curr Opin Lipidol. 2013 Feb;24(1):78-85. doi: 10.1097/MOL.0b013e32835b4431.

Abstract

Purpose of review: This article reviews the evidence linking gut bacteria, endotoxin, and its circulating levels with inflammatory induced obesity and metabolic disease (metabolic endotoxaemia).

Recent findings: Gut flora analyses have allowed gut microbiota signatures (GMS) to be observed in animal studies of obesity/metabolic disease. In these studies, specific GMS result in a change in obesity and metabolic disease state whereas in humans, analysis remains unclear. Serum studies, examining metabolic endotoxaemia as a biomarker, appear to link long-term cardiovascular disease and type 2 diabetes mellitus (T2DM) through activation of inflammatory pathways. More recent studies note the importance of diet, which shows the dramatic rise in endotoxin following acute or long-term high-fat diet, with the effects exacerbated in T2DM.

Summary: Gut flora appears to act as an important determinant in the pathogenesis of inflammatory induced obesity/T2DM. Endotoxin may act as the systemic insult, impacted by a high-fat diet, which may regulate this effect, combined with an altered GMS. As such, clinical and dietary intervention to affect this process - on the gut flora, the 'leaky' mucosal membrane and endotoxin coupled lipid absorption or removal of circulating endotoxin - could reduce the progression of inflammatory induced metabolic disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bacteria / growth & development
  • Bacteria / immunology
  • Bacteria / pathogenicity
  • Biomarkers / metabolism
  • Diabetes Mellitus, Type 2 / pathology
  • Diet, High-Fat / adverse effects*
  • Endotoxemia / immunology
  • Endotoxemia / metabolism*
  • Endotoxemia / microbiology
  • Gastrointestinal Tract / immunology
  • Gastrointestinal Tract / metabolism
  • Gastrointestinal Tract / microbiology*
  • Humans
  • Inflammation / microbiology*
  • Inflammation / pathology
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / microbiology
  • Lipid Metabolism
  • Lipopolysaccharides / immunology
  • Metagenome
  • Obesity / immunology
  • Obesity / microbiology
  • Obesity / pathology
  • Risk Factors

Substances

  • Biomarkers
  • Lipopolysaccharides