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发酵桔梗提取物抑制3T3-L1脂肪细胞和高脂饮食诱导的肥胖小鼠中的脂质积累。

Fermented Platycodon grandiflorum Extract Inhibits Lipid Accumulation in 3T3-L1 Adipocytes and High-Fat Diet-Induced Obese Mice.

作者信息

Huang Yu-Hua, Jung Da-Woon, Lee Ok-Hwan, Kang Il-Jun

机构信息

1 Department of Food Science and Nutrition, Hallym University , Chuncheon, Korea.

2 Department of Food Science and Biotechnology, Kangwon National University , Chuncheon, Korea.

出版信息

J Med Food. 2016 Nov;19(11):1004-1014. doi: 10.1089/jmf.2016.3805. Epub 2016 Oct 28.

Abstract

The aim of this study was to investigate whether fermented Platycodon grandiflorum (FPG) inhibits lipid accumulation in 3T3-L1 adipocytes and mice with high-fat diet (HFD)-induced obesity. We evaluated the effect of FPG on antiadipogenic activity via regulation of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα), as well as protein expression of their target genes, fatty acid binding protein 4 (FABP4). We further examined the antiobesity effects of FPG on HFD-induced obesity in mice. The FPG was orally administered to mice with a HFD at 50, 100, or 200 mg/kg/day for 8 weeks. Our results show that FPG significantly inhibited fat accumulation during 3T3-L1 adipogenesis through downregulating adipogenic transcript factors. Moreover, FPG markedly reduced the final body weight with a decrease in epididymal adipose tissue mass and adipocyte size compared with the untreated HFD-induced group. The effects of FPG on HFD-induced obesity were primarily responsible for inhibiting adipogenesis in adipose tissue and regulating lipid metabolism, such as through lipogenesis and fatty acid oxidation. Additionally, FPG ameliorated serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels. Hence, FPG may be an alternative treatment for controlling obesity through downregulating lipid accumulation.

摘要

本研究旨在探讨发酵桔梗(FPG)是否能抑制3T3-L1脂肪细胞和高脂饮食(HFD)诱导的肥胖小鼠中的脂质积累。我们通过调节过氧化物酶体增殖物激活受体γ(PPARγ)和CCAAT/增强子结合蛋白α(C/EBPα)及其靶基因脂肪酸结合蛋白4(FABP4)的蛋白表达,评估了FPG对抗脂肪生成活性的影响。我们进一步研究了FPG对HFD诱导的小鼠肥胖的抗肥胖作用。将FPG以50、100或200mg/kg/天的剂量口服给予HFD喂养的小鼠,持续8周。我们的结果表明,FPG通过下调脂肪生成转录因子,在3T3-L1脂肪生成过程中显著抑制脂肪积累。此外,与未处理的HFD诱导组相比,FPG显著降低了最终体重,附睾脂肪组织质量和脂肪细胞大小也有所减少。FPG对HFD诱导的肥胖的影响主要是通过抑制脂肪组织中的脂肪生成和调节脂质代谢,如通过脂肪生成和脂肪酸氧化。此外,FPG改善了血清总胆固醇、甘油三酯和低密度脂蛋白胆固醇水平。因此,FPG可能是一种通过下调脂质积累来控制肥胖的替代治疗方法。

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