Abstract：
:Mitochondrial fatty acid oxidation provides an important energy source for cellular metabolism, and decreased mitochondrial fatty acid oxidation has been implicated in the pathogenesis of type 2 diabetes. Paradoxically, mice with an inherited deficiency of the mitochondrial fatty acid oxidation enzyme, very long-chain acyl-CoA dehydrogenase (VLCAD), were protected from high-fat diet-induced obesity and liver and muscle insulin resistance. This was associated with reduced intracellular diacylglycerol content and decreased activity of liver protein kinase Cvarepsilon and muscle protein kinase Ctheta. The increased insulin sensitivity in the VLCAD(-/-) mice were protected from diet-induced obesity and insulin resistance due to chronic activation of AMPK and PPARalpha, resulting in increased fatty acid oxidation and decreased intramyocellular and hepatocellular diacylglycerol content.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Zhang D,Christianson J,Liu ZX,Tian L,Choi CS,Neschen S,Dong J,Wood PA,Shulman GIdoi
10.1016/j.cmet.2010.03.012subject
Has Abstractpub_date
2010-05-05 00:00:00pages
402-11issue
5eissn
1550-4131issn
1932-7420pii
S1550-4131(10)00082-3journal_volume
11pub_type
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