首页> 外文期刊>Natural Products and Bioprospecting >Pyrocincholic acid 3β-O-β-d-quinovopyranosyl-28-O-β-d-glucopyranoside suppresses adipogenesis and regulates lipid metabolism in 3T3-L1 adipocytes
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Pyrocincholic acid 3β-O-β-d-quinovopyranosyl-28-O-β-d-glucopyranoside suppresses adipogenesis and regulates lipid metabolism in 3T3-L1 adipocytes

机译:吡喹啉酸3β-O-β-d-喹诺吡喃糖基-28-O-β-d-吡喃葡萄糖苷抑制3T3-L1脂肪细胞的脂肪形成并调节脂质代谢

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Obesity is crucially involved in many metabolic diseases, such as type 2 diabetes, cardiovascular disease and cancer. Regulating the number or size of adipocytes has been suggested to be a potential treatment for obesity. In this study, we investigated the effect of pyrocincholic acid 3β-O-β-d-quinovopyranosyl-28-O-β-d-glucopyranoside (PAQG), a 27-nor-oleanolic acid saponin extracted from Metadina trichotoma, on adipogenesis and lipid metabolism in 3T3-L1 adipocytes. The 3T3-L1 pre-adipocytes were incubated with vehicle or PAQG for 6?days in differentiation process. PAQG significantly reduced the adipogenesis, adiponectin secretion and the expression level of key transcription factors related to adipogenesis, such as PPARγ, C/EBPβ, C/EBPα, and FABP4. Moreover, PAQG increased the levels of FFA and glycerol in medium and reduced TG level in mature adipocytes. Interestingly, PAQG not only promoted the activation of AMPK and genes involved in fatty oxidation including PDK4 and CPT1a, but also inhibited those genes involved in fatty acid biosynthesis, such as SREBP1c, FAS, ACCα and SCD1. In conclusion, PAQG inhibits the differentiation and regulates lipid metabolism of 3T3-L1 cells via AMPK pathway, suggesting that PAQG may be a novel and promising natural product for the treatment of obesity and hyperlipidemia.Graphical AbstractOpen image in new window
机译:肥胖与许多代谢性疾病至关重要,例如2型糖尿病,心血管疾病和癌症。已经建议调节脂肪细胞的数量或大小是肥胖症的潜在治疗方法。在这项研究中,我们研究了从麦地那非(Metadina trichotoma)提取的27-去甲油酸皂苷中的吡喹啉酸3β-O-β-d-喹啉吡喃糖基-28-O-β-d-吡喃葡萄糖苷(PAQG)对脂肪形成和3T3-L1脂肪细胞中的脂质代谢。在分化过程中,将3T3-L1前脂肪细胞与媒介物或PAQG孵育6天。 PAQG显着降低了脂肪形成,脂联素分泌以及与脂肪形成相关的关键转录因子(如PPARγ,C /EBPβ,C /EBPα和FABP4)的表达水平。此外,PAQG可增加培养基中FFA和甘油的水平,并降低成熟脂肪细胞中TG的水平。有趣的是,PAQG不仅促进了AMPK和涉及脂肪氧化的基因(包括PDK4和CPT1a)的活化,而且还抑制了与脂肪酸生物合成有关的那些基因,例如SREBP1c,FAS,ACCα和SCD1。总之,PAQG通过AMPK途径抑制3T3-L1细胞的分化并调节脂质代谢,这表明PAQG可能是治疗肥胖和高脂血症的一种新颖且有希望的天然产物。

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