期刊
NUTRITION REVIEWS
卷 65, 期 6, 页码 S13-S23出版社
INT LIFE SCIENCES INST NORTH AMERICA
DOI: 10.1301/nr.2007.jun.S13-S23
关键词
fructose; hepatic lipogenesis; insulin resistance; JNK; metabolic syndrome; obesity; NFkB; TNF-alpha
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.
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