Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms

Nutr Rev. 2007 Jun;65(6 Pt 2):S13-23. doi: 10.1111/j.1753-4887.2007.tb00322.x.


Emerging evidence suggests that increased dietary consumption of fructose in Western society may be a potentially important factor in the growing rates of obesity and the metabolic syndrome. This review will discuss fructose-induced perturbations in cell signaling and inflammatory cascades in insulin-sensitive tissues. In particular, the roles of cellular signaling molecules including nuclear factor kappa B (NFkB), tumor necrosis factor alpha (TNF-alpha), c-Jun amino terminal kinase 1 (JNK-1), protein tyrosine phosphatase 1B (PTP-1B), phosphatase and tensin homolog deleted on chromosome ten (PTEN), liver X receptor (LXR), farnesoid X receptor (FXR), and sterol regulatory element-binding protein-1c (SREBP-1c) will be addressed. Considering the prevalence and seriousness of the metabolic syndrome, further research on the underlying molecular mechanisms and preventative and curative strategies is warranted.

Publication types

  • Review

MeSH terms

  • Animals
  • Disease Models, Animal
  • Fructose / administration & dosage*
  • Humans
  • Metabolic Syndrome / etiology
  • Metabolic Syndrome / metabolism*
  • Obesity / etiology
  • Obesity / metabolism*
  • Signal Transduction / drug effects
  • Sweetening Agents / administration & dosage*


  • Sweetening Agents
  • Fructose