Guo Yuan-Ri, Choung Se-Young
1 Department of Preventive Pharmacy and Toxicology, College of Pharmacy, Kyung Hee University , Seoul, Republic of Korea.
2 Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University , Seoul, Republic of Korea.
J Med Food. 2017 Jan;20(1):46-55. doi: 10.1089/jmf.2016.3811.
We previously showed that Aster spathulifolius Maxim extract (ASE) reduced body weight gain and serum and liver lipid levels and significantly suppressed serum insulin and leptin concentrations in high-fat diet (HFD)-induced obese rats. Germacrone (GM) was identified as a potent bioactive constituent of ASE. In this study, we hypothesized that GM can attenuate hyperlipidemia by alleviating fatty acid (FA) synthesis/uptake and improve lipid metabolism by stimulating FA β-oxidation in HFD-induced obese C57BL/6J mice. To induce obesity, mice were fed an HFD for 6 weeks, while control mice were fed a commercial standard diet. The mice were allocated to six groups and fed either a normal diet, HFD, HFD with GM (5, 10, and 20 mg/kg), or HFD with 200 mg/kg Garcinia cambogia extract for 30 days. In the GM groups, body weight gain, visceral fat pad weight, fasting plasma glucose, serum insulin and leptin, and serum, as well as hepatic lipid, levels were attenuated. Transcriptional factors related to lipid metabolism, such as AMP-activated protein kinase α, sterol regulatory element-binding protein (SREBP) 1, SREBP 2, acetyl-CoA carboxylase, peroxisome proliferator-activated receptor (PPAR)-α, PPAR-γ, FA synthase, and carnitine palmitoyltransferase 1, showed higher expression in the GM groups. In summary, GM may help attenuate hyperlipidemia by suppressing FA synthesis and uptake by inhibiting SREBP signaling pathway activation and improve lipid metabolism by stimulating FA β-oxidation by activating the AMPKα signaling pathway in HFD-induced obesity.
我们之前的研究表明，紫菀提取物（ASE）可减少高脂饮食（HFD）诱导的肥胖大鼠的体重增加、血清和肝脏脂质水平，并显著抑制血清胰岛素和瘦素浓度。吉马酮（GM）被鉴定为ASE的一种有效生物活性成分。在本研究中，我们假设GM可通过减轻脂肪酸（FA）合成/摄取来减轻高脂血症，并通过刺激高脂饮食诱导的肥胖C57BL/6J小鼠的FAβ-氧化来改善脂质代谢。为诱导肥胖，给小鼠喂食高脂饮食6周，而对照小鼠喂食商业标准饮食。将小鼠分为六组，分别喂食正常饮食、高脂饮食、含GM（5 mg/kg、10 mg/kg和20 mg/kg）的高脂饮食或含200 mg/kg藤黄果提取物的高脂饮食，持续30天。在GM组中，体重增加、内脏脂肪垫重量、空腹血糖、血清胰岛素和瘦素以及血清和肝脏脂质水平均有所减轻。与脂质代谢相关的转录因子，如AMP激活的蛋白激酶α、固醇调节元件结合蛋白（SREBP）-1、SREBP-2、乙酰辅酶A羧化酶、过氧化物酶体增殖物激活受体（PPAR）-α、PPAR-γ、脂肪酸合酶和肉碱棕榈酰转移酶1，在GM组中表达较高。总之，GM可能通过抑制SREBP信号通路激活来抑制FA合成和摄取，从而有助于减轻高脂血症，并通过激活AMPKα信号通路刺激FAβ-氧化来改善高脂饮食诱导的肥胖中的脂质代谢。
