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矢车菊素-3-葡萄糖苷对 3T3-L1 前体脂肪细胞和原代白色脂肪细胞的抗脂肪生成作用。

Anti-Adipogenic Effects of Delphinidin-3---Glucoside in 3T3-L1 Preadipocytes and Primary White Adipocytes.

机构信息

Department of Food and Nutrition, Gachon University, Gyeonggi-do 13120, Korea.

出版信息

Molecules. 2019 May 14;24(10):1848. doi: 10.3390/molecules24101848.

Abstract

Delphinidin-3---glucoside (D3G) is a health-promoting anthocyanin whose anti-obesity activity has not yet been thoroughly investigated. We examined the effects of D3G on adipogenesis and lipogenesis in 3T3-L1 adipocytes and primary white adipocytes using real-time RT-PCR and immunoblot analysis. D3G significantly inhibited the accumulation of lipids in a dose-dependent manner without displaying cytotoxicity. In the 3T3-L1 adipocytes, D3G downregulated the expression of key adipogenic and lipogenic markers, which are known as peroxisome proliferator-activated receptor gamma (PPARγ), sterol regulatory element-binding transcription factor 1 (SREBP1), CCAAT/enhancer-binding protein alpha (C/EBPα), and fatty acid synthase (FAS). Moreover, the relative protein expression of silent mating type information regulation 2 homolog 1 (SIRT1) and carnitine palmitoyltransferase-1 (CPT-1) were increased, alongside reduced lipid levels and the presence of several small lipid droplets. Furthermore, D3G increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), which suggests that D3G may play a role in AMPK and ACC activation in adipocytes. Our data indicate that D3G attenuates adipogenesis and promotes lipid metabolism by activating AMPK-mediated signaling, and, hence, could have a therapeutic role in the management and treatment of obesity.

摘要

飞燕草素-3---葡萄糖苷(D3G)是一种具有促进健康作用的花色苷,其抗肥胖活性尚未得到彻底研究。我们使用实时 RT-PCR 和免疫印迹分析,研究了 D3G 对 3T3-L1 脂肪细胞和原代白色脂肪细胞的脂肪生成和脂生成的影响。D3G 以剂量依赖性方式显著抑制脂质积累,而没有显示细胞毒性。在 3T3-L1 脂肪细胞中,D3G 下调了已知的过氧化物酶体增殖物激活受体γ(PPARγ)、固醇调节元件结合转录因子 1(SREBP1)、CCAAT/增强子结合蛋白α(C/EBPα)和脂肪酸合酶(FAS)等关键脂肪生成和脂生成标记物的表达。此外,沉默交配型信息调节 2 同源物 1(SIRT1)和肉碱棕榈酰基转移酶-1(CPT-1)的相对蛋白表达增加,同时脂质水平降低,存在几个小脂质滴。此外,D3G 增加了腺苷单磷酸激活蛋白激酶(AMPK)和乙酰辅酶 A 羧化酶(ACC)的磷酸化,这表明 D3G 可能在脂肪细胞中 AMPK 和 ACC 激活中发挥作用。我们的数据表明,D3G 通过激活 AMPK 介导的信号通路来减轻脂肪生成并促进脂质代谢,因此在肥胖症的管理和治疗中可能具有治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b2/6571603/cdd50f40fcf9/molecules-24-01848-g001.jpg

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