Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul, Korea.
Planta Med. 2012 Sep;78(14):1536-42. doi: 10.1055/s-0032-1315147. Epub 2012 Aug 7.
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 α (AMPKα) 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), and Western 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 γ2 (PPARγ2) and CCAAT/enhancer binding protein α (C/EBPα), which functions via AMPK signaling, in vitro. PD reduced both body weight and fat volume; consequently, lipid metabolism was improved by increasing AMPKα, similar to AICAR, and reduced PPARγ2 and C/EBPα 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.
远志酸（PD）已被报道可在体内控制肥胖。本研究主要探讨了 PD 的分子机制，重点研究了 PD 通过 AMP 激活的蛋白激酶α（AMPKα）在脂肪细胞中降低脂肪生成因子表达的能力，以及预防高脂肪饮食诱导的肥胖 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 blot 测定 3T3-L1 细胞中脂质积累的抑制作用。为了确定体内的抗肥胖作用，一组小鼠给予正常饮食，另一组给予高脂肪饮食 8 周。然后将高脂肪饮食的小鼠分为三组：氨基咪唑甲酰胺核苷酸（AICAR）、载体和 PD。PD 通过 AMPK 信号通路抑制脂肪生成信号转录因子，如过氧化物酶体增殖物激活受体γ2（PPARγ2）和 CCAAT/增强子结合蛋白α（C/EBPα），在体外显著减少脂肪积累。PD 降低了体重和脂肪体积；因此，通过增加 AMPKα，类似于 AICAR，改善了脂质代谢，并降低了脂肪组织中 PPARγ2 和 C/EBPα 的表达。结果表明，PD 可用于降低与 AMPK 途径相关的脂肪生成因子的表达。因此，PD 可通过下调脂质积累来控制肥胖。
