期刊
CELLULAR SIGNALLING
卷 24, 期 12, 页码 2329-2336出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2012.07.022
关键词
Adipogenesis; AMPK; Coenzyme Q10; Fatty acid oxidation; PPAR alpha
类别
资金
- National Research Foundation of Korea
- Korea government [2010-0011053]
- National Research Foundation of Korea [2010-0011053] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Coenzyme Q10(CoQ10) is a known anti-adipogenic factor. However, the mechanism by which CoQ10 acts is unclear. In this study, we found that CoQ10 increased the phosphorylation of AMP-activated protein kinase (AMPK) in 3T3-L1preadipocytes. CoQ10 induced an increase in cytoplasmic calcium concentrations, which is reflected by increased Fluo-3 intensity under confocal microscopy recording. Either inhibition of Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) or knock-down CaMKK blocked CoQ10-induced AMPK phosphorylation, suggesting the involvement of calcium in CoQ10-mediated AMPK signaling. CoQ10 also increased the expression of peroxisome proliferator-activated receptor alpha (PPAR alpha) at both the mRNA and protein levels. Knock down of AMPK with siRNA or inhibition of AMPK using an AMPK inhibitor compound C blocked CoQ10-induced expression of PPAR alpha, indicating that AMPK plays a critical role in PPAR alpha induction. In addition, CoQ10 increased fatty acid oxidation in 3T3-L1preadipocytes. The promoter activity of PPAR alpha was increased by CoQ10 in an AMPK-dependent fashion. Moreover, the induction of acyl-CoA oxidase (ACO), a target gene of PPAR alpha, was blocked under the PPAR alpha knock down condition. Furthermore, treatment with CoQ10 blocked differentiation-induced adipogenesis. This blockade was not observed under the PPAR alpha knock-down condition. Collectively, these results demonstrate that CoQ10 induces PPAR alpha expression via the calcium-mediated AMPK signal pathway and suppresses differentiation-induced adipogenesis. (c) 2012 Elsevier Inc. All rights reserved.
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