Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms.
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.
Rutledge
Angela C
AC
Department of Clinical Biochemistry and Molecular Structure and Function, University of Toronto, Ontario, Canada.
Adeli
Khosrow
K
D000818:Animals; D004195:Disease Models, Animal; D005632:Fructose / Q000008:administration & dosage*; D006801:Humans; D024821:Metabolic Syndrome / Q000209:etiology / Q000378:metabolism*; D009765:Obesity / Q000209:etiology / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D013549:Sweetening Agents / Q000008:administration & dosage*
D013549:Sweetening Agents; D005632:Fructose