Importance of TNF-alpha and leptin in obesity and insulin resistance: a hypothesis on the impact of physical exercise

Exerc Immunol Rev. 1998:4:77-94.

Abstract

Obesity is associated with an increased incidence of insulin resistance, dyslipoproteinemia, and hypercoagulability. In a more recently established hypothesis of body weight control and regulation of metabolism, the adipocyte secretes leptin and locally expresses TNF-alpha, the latter being responsible for the expression of metabolic cardiovascular risk factors. TNF-a mRNA expression and TNF-alpha protein are greatly increased in adipose tissue from obese animals and humans. Elevated TNF-alpha expression induces insulin resistance by downregulating the tyrosine kinase activity of the insulin receptor and decreasing the expression of GLUT-4 glucose transporters. TNF-alpha also reduces lipoprotein lipase activity in white adipocytes, stimulates hepatic lipolysis, and increases plasminogen activator inhibitor-1 content in adipocytes. Moreover, adipocytes secrete leptin, a molecule with a secondary cytokine structure whose concentrations correlate with the amount of fat tissue. Increased leptin levels downregulate appetite and increase sympathetic activity and thermogenesis in the hypothalamus. Diet-induced weight loss reduces adipose TNF-alpha expression and serum leptin levels and is associated with improved insulin sensitivity and lipid metabolism. Although exercise has also been shown to reduce leptin levels, an influence on TNF-a expression in adipocytes or muscle cells has not yet been demonstrated.

Publication types

  • Review

MeSH terms

  • Animals
  • Arteriosclerosis / immunology
  • Coronary Disease / immunology
  • Diet
  • Exercise*
  • Humans
  • Insulin Resistance / physiology*
  • Leptin
  • Obesity*
  • Proteins / metabolism
  • Proteins / physiology*
  • Risk Factors
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / physiology*
  • Weight Loss

Substances

  • Leptin
  • Proteins
  • Tumor Necrosis Factor-alpha