Lipid signals and insulin resistance

被引:36
|
作者
Zhang, Chongben [1 ]
Klett, Eric L. [2 ]
Coleman, Rosalind A. [1 ]
机构
[1] Univ N Carolina, Dept Nutr, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Med, Chapel Hill, NC 27599 USA
关键词
acyl-CoA; ceramide; diacylglycerol; lysophosphatidic acid; phosphatidic acid; PROTEIN-KINASE-C; FATTY-ACID OXIDATION; HEPATIC STEATOSIS; PKC-ZETA; DIACYLGLYCEROL KINASE; RECEPTOR SUBSTRATE-1; MUSCLE; METABOLISM; ACTIVATION; INHIBITION;
D O I
10.2217/clp.13.67
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The metabolic syndrome, a cluster of metabolic derangements that include obesity, glucose intolerance, dyslipidemia and hypertension, is a major risk factor for cardiovascular disease. Insulin resistance has been proposed to be the common feature that links obesity to the metabolic syndrome, but the mechanism remains obscure. Although the excess content of triacylglycerol in muscle and liver is highly associated with insulin resistance in these tissues, triacylglycerol itself is not causal but merely a marker. Thus, attention has turned to the accumulation of cellular lipids known to have signaling roles. This review will discuss recent progress in understanding how glycerolipids and related lipid intermediates may impair insulin signaling.
引用
收藏
页码:659 / 667
页数:9
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