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Daidzein stimulates fatty acid-induced fat deposition in C2C12 myoblast cells via the G protein-coupled receptor 30 pathway
Animal Biotechnology ( IF 3.7 ) Pub Date : 2020-11-08 , DOI: 10.1080/10495398.2020.1842749
Chengjian Zhou 1 , Ping Li 1 , Meihong Han 1 , Xuejun Gao 1
Affiliation  

Abstract

Fat deposition in skeletal muscle is an important aspect of improving meat quality. Isoflavones can promote animal anabolism, but whether and how they regulate muscle fat deposition remain largely unclear. In this study, we explored the role and corresponding molecular mechanism of one of the major isoflavones, daidzein, in fat deposition in C2C12 myoblast cells. In the absence of fatty acids (FAs), daidzein did not promote triglyceride synthesis and lipid droplet formation in cells but increased sterol regulatory element-binding protein 1c (SREBP-1c) expression and maturation. In the presence of FAs, daidzein enhanced FAs-induced fat deposition and the SREBP-1c signaling. Daidzein promoted FAs-induced nuclear factor κB1 (NFκB1) phosphorylation and activated the SREBP-1c signaling in a PI3K-dependent manner. G protein-coupled receptor 30 (GPR30) knockdown but not estrogen receptor α (ERα) knockdown blocked the stimulation of daidzein on the PI3K-NFκB1-SREBP-1c signaling pathway, while both knockdown did not affect the stimulation of FAs on this signaling. qRT-PCR and ChIP-qPCR further detected that daidzein stimulated NFκB1-targeted SREBP-1c transcription. Daidzein did not affect ERα expression in cells, but it stimulated GPR30 expression and cytoplasmic localization. These results reveal that daidzein promotes FAs-induced fat deposition through the GPR30 signaling in C2C12 myoblast cells.



中文翻译:

黄豆苷元通过 G 蛋白偶联受体 30 通路刺激 C2C12 成肌细胞中脂肪酸诱导的脂肪沉积

摘要

骨骼肌中的脂肪沉积是改善肉质的一个重要方面。异黄酮可以促进动物合成代谢,但它们是否以及如何调节肌肉脂肪沉积仍不清楚。在这项研究中,我们探讨了一种主要的异黄酮黄豆苷元在 C2C12 成肌细胞脂肪沉积中的作用和相应的分子机制。在没有脂肪酸 (FAs) 的情况下,黄豆苷元不会促进细胞中甘油三酯的合成和脂滴的形成,但会增加甾醇调节元件结合蛋白 1c (SREBP-1c) 的表达和成熟。在 FAs 存在下,黄豆苷元增强了 FAs 诱导的脂肪沉积和 SREBP-1c 信号传导。Daidzein 促进 FAs 诱导的核因子 κB1 (NFκB1) 磷酸化并以 PI3K 依赖性方式激活 SREBP-1c 信号传导。G 蛋白偶联受体 30 (GPR30) 敲低而不是雌激素受体 α (ERα) 敲低阻断了黄豆苷元对 PI3K-NFκB1-SREBP-1c 信号通路的刺激,而两种敲低均不影响 FA 对该信号通路的刺激。qRT-PCR 和 ChIP-qPCR 进一步检测到黄豆苷元刺激 NFκB1 靶向SREBP-1c转录。黄豆苷元不影响细胞中 ERα 的表达,但它刺激 GPR30 的表达和细胞质定位。这些结果表明,黄豆苷元通过 C2C12 成肌细胞中的 GPR30 信号传导促进 FAs 诱导的脂肪沉积。

更新日期:2020-11-08
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