Platycodin D Inhibits Lipogenesis through AMPKα-PPARγ2 in 3T3-L1 Cells and Modulates Fat Accumulation in Obese Mice
Platycodin D Inhibits Lipogenesis through AMPKα-PPARγ2 in 3T3-L1 Cells and Modulates Fat Accumulation in Obese Mice
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DOI：
10.1055/s-0032-1315147
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发表时间：
2012-09-01
期刊：
影响因子：
2.7
通讯作者：
Kim, Yeong Shik
中科院分区：
文献类型：
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作者：
Lee, Eun Jeong;Kang, Minseok;Kim, Yeong Shik
据报道，桔梗皂苷 D (PD) 可以在体内控制肥胖。本研究探讨了PD的分子机制，重点关注其通过AMP激活蛋白激酶α（AMPKα）降低脂肪细胞中脂肪形成因子表达的能力，以及其防止高脂饮食诱导的肥胖C57BL/6小鼠腹部脂肪堆积的能力。通过油红O染色、逆转录聚合酶链反应(RT-PCR)和Western blotting检测3T3-L1细胞中脂质积累的抑制作用。为了确定体内的抗肥胖效果，一组小鼠接受正常饮食，而另一组小鼠则接受高脂肪饮食，为期 8 周。然后将高脂肪饮食小鼠分配到三个亚组之一：氨基咪唑甲酰胺核糖核苷酸（AICAR）、载体和PD。 PD 通过抑制脂肪形成信号转录因子，例如过氧化物酶体增殖物激活受体 γ 2 (PPAR γ 2) 和 CCAAT/增强子结合蛋白 α (C/EBP α)（体外通过 AMPK 信号传导发挥作用），显着减少脂肪积累。 PD降低了体重和脂肪量；因此，与 AICAR 相似，通过增加 AMPK α 来改善脂质代谢，并减少脂肪组织中 PPAR γ 2 和 C/EBP α 的表达。结果表明，PD 可用于降低与 AMPK 通路相关的脂肪形成因子的表达。因此，PD 可能是通过下调脂质积累来控制肥胖的替代疗法。
Platycodin D (PD) has been reported to control obesity in vivo. This study investigated the molecular mechanism of PD, focusing on its ability to decrease the expression of adipogenic factors through AMP-activated protein kinase alpha (AMPK alpha) in adipocytes and its ability to prevent abdominal fat accumulation in high-fat diet-induced obese C57BL/6 mice. The inhibitory effect of lipid accumulation in 3T3-L1 cells was measured by Oil Red O staining, reverse transcription-polymerase chain reaction (RT-PCR), andWestern blotting. To determine the antiobesity effect in vivo, one group of mice were given a normal diet and the others were fed a high-fat diet for 8 weeks. The high-fat diet mice were then assigned to one of three subgroups: aminoimidazole carboxamide ribonucleotide (AICAR), vehicle, and PD. PD significantly reduced fat accumulation by inhibiting adipogenic signal transcriptional factors, such as peroxisome proliferator-activated receptor gamma 2 (PPAR gamma 2) and CCAAT/enhancer binding protein alpha (C/EBP alpha), which functions via AMPK signaling, in vitro. PD reduced both body weight and fat volume; consequently, lipid metabolism was improved by increasing AMPK alpha, similar to AICAR, and reduced PPAR gamma 2 and C/EBP alpha expression in adipose tissue. The results suggested that PD could be used to decrease the expression of adipogenic factors related to the AMPK pathway. Hence, PD could be an alternative treatment for controlling obesity by downregulating lipid accumulation.