The anti-obesity effect of quercetin is mediated by the AMPK and MAPK signaling pathways
The anti-obesity effect of quercetin is mediated by the AMPK and MAPK signaling pathways
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DOI：
10.1016/j.bbrc.2008.06.077
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发表时间：
2008-09-05
影响因子：
3.1
通讯作者：
Ha, Taleyoul
中科院分区：
文献类型：
--
作者：
Ahn, Jiyun;Lee, Hyunjung;Ha, Taleyoul
槲皮素是最丰富的黄酮类化合物，被认为对与氧化应激相关的多种疾病的发病机制具有保护作用。在本研究中，我们研究了槲皮素影响3 T3-L1细胞脂肪生成和凋亡的分子机制。3 T3-L1前脂肪细胞暴露于槲皮素导致脂肪生成减弱，脂肪生成相关因子和酶的表达降低。此外，槲皮素暴露上调磷酸化腺苷一磷酸活化蛋白激酶（AMPK）及其底物，乙酰辅酶A羧化酶（ACC）的水平。用槲皮素处理3 T3-L1脂肪细胞导致细胞凋亡的诱导和伴随的ERK和JNK磷酸化的减少。综上所述，这些数据表明，槲皮素通过激活3 T3-L1前脂肪细胞中的AMPK信号通路来发挥抗脂肪生成活性，而槲皮素诱导的成熟脂肪细胞的凋亡是通过调节ERK和JNK通路来介导的，这两条通路在凋亡过程中起关键作用。皇冠版权所有（C）2008由爱思唯尔公司出版。All rights reserved.
Quercetin is the most abundant flavonoid and is assumed to have protective roles against the pathogenesis of multiple diseases associated with oxidative stress. In the present study, we investigated the molecular mechanisms by which quercetin affects adipogenesis and apoptosis in 3T3-L1 cells. The exposure of 3T3-L1 preadipocytes to quercetin resulted in attenuated adipogenesis and decreased expression of adipogenesis-related factors and enzymes. Moreover, quercetin exposure up-regulated the levels of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase (ACC). Treatment of 3T3-L1 adipocytes with quercetin resulted in the induction of apoptosis and a concomitant decrease in ERK and JNK phosphorylation. Taken together, these data indicate that quercetin exerts anti-adipogenesis activity by activating the AMPK signal pathway in 3T3-L1 preadipocytes, while the quercetin-induced apoptosis of mature adipocytes was mediated by modulation of the ERK and JNK pathways, which play pivotal roles during apoptosis. Crown Copyright (C) 2008 Published by Elsevier Inc. All rights reserved.