Toll-like receptors, inflammation, metabolism and obesity

Arch Physiol Biochem. 2011 Jul;117(3):151-64. doi: 10.3109/13813455.2011.562514. Epub 2011 May 23.

Abstract

Obesity is a highly prevalent health problem in Western countries that leads to many important diseases such as type 2 diabetes and metabolic syndrome being now considered an inflammatory chronic disease. Adipocytes are no longer considered passive cells storing fat since they are major producers of inflammatory cytokines during obesity. Adipocytes and macrophages share many biological properties including the synthesis of similar molecules regulating inflammation. Fatty acid levels are elevated in obesity and induce inflammatory pathways by yet a mostly unknown mechanism, leading to the development of insulin and leptin resistance. Recent studies suggest that these effects could be mediated through the activation of toll-like receptors (TLR). TLR signalling pathways might contribute to the development of obesity-associated insulin resistance, thus representing a connection between innate immunity and metabolism. Here, we summarize the recent evidence for the important role that TLRs play in adipose tissue, obesity and insulin resistance.

Publication types

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

MeSH terms

  • Adipocytes / immunology
  • Adipose Tissue / immunology
  • Animals
  • Cytokines / immunology
  • Diabetes Mellitus, Type 2 / immunology
  • Humans
  • Inflammation / immunology*
  • Insulin Resistance / immunology
  • Leptin / metabolism
  • Macrophages / immunology
  • Metabolic Syndrome / immunology
  • Obesity / immunology*
  • Signal Transduction / immunology
  • Toll-Like Receptors / immunology*

Substances

  • Cytokines
  • Leptin
  • Toll-Like Receptors