乙酸在乳脂合成过程中通过乳腺上皮细胞中的 PI3K-AKT-SP1 信号传导上调 GPR43 表达和功能,Journal of Agricultural and Food Chemistry

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乙酸在乳脂合成过程中通过乳腺上皮细胞中的 PI3K-AKT-SP1 信号传导上调 GPR43 表达和功能
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2023-10-23 , DOI: 10.1021/acs.jafc.3c00965
Yang Yang ₁ , Chuanping Liu ₁ , Caiyan Zhang ₁ , Ziru Xu ₁ , Li Zhang ₂ , Yingjun Cui ₂ , Chunmei Wang ₂ , Ye Lin _{1,

2} , Xiaoming Hou ₁

Affiliation

本研究调查了醋酸盐诱导孤儿 G 蛋白偶联受体 43 (GPR43) 表达和乳脂产生的机制。用醋酸盐处理奶牛乳腺上皮细胞，分别通过气相色谱和定量聚合酶链反应（qPCR）测定GPR43对醋酸盐摄取和脂肪生成相关基因表达的影响。RNAi、抑制剂处理和荧光素酶测定用于确定磷酸肌醇 3-激酶-蛋白激酶 B-特异性蛋白 1 (PI3K-AKT-SP1) 信号传导对乙酸诱导的 GPR43 表达和功能的影响。结果表明，GPR43在泌乳牛乳腺组织中高表达，与乳脂合成有关。12 mM 乙酸盐显着增加奶牛乳腺上皮细胞中 GPR43 的表达。在醋酸盐处理的细胞中，GPR43过表达显着增加细胞对醋酸盐的摄取、细胞内三酰甘油 (TAG) 含量以及醋酸盐诱导的脂肪生成基因表达。乙酸激活 PI3K-AKT 信号传导并促进 SP1 从细胞质转位到细胞核，其中 SP1 与GPR43启动子结合并上调GPR43转录。此外，乙酸盐激活 PI3K-AKT-SP1 促进 GPR43 从细胞质运输到质膜。总之，乙酸盐通过乳腺上皮细胞中的 PI3K-AKT-SP1 信号传导上调 GPR43 的表达和功能，从而增加乳脂合成。这些结果为改善乳脂合成提供了实验策略，这对乳制品行业很重要。

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Acetate Upregulates GPR43 Expression and Function via PI3K-AKT-SP1 Signaling in Mammary Epithelial Cells during Milk Fat Synthesis

This study investigated the mechanism underlying acetate-induced orphan G-protein-coupled receptor 43 (GPR43) expression and milk fat production. The mammary epithelial cells of dairy cows were treated with acetate, and the effects of GPR43 on acetate uptake and the expression of lipogenesis-related genes were determined by gas chromatography and quantitative polymerase chain reaction (qPCR), respectively. RNAi, inhibitor treatment, and luciferase assay were used to determine the effect of phosphoinositide 3-kinase-protein kinase B-specificity protein 1 (PI3K-AKT-SP1) signaling on acetate-induced GPR43 expression and function. The results showed that GPR43 was highly expressed in lactating cow mammary tissues, which was related to milk fat synthesis. 12 mM acetate significantly increased the GPR43 expression in mammary epithelial cells of dairy cows. In acetate-treated cells, GPR43 overexpression significantly increased the cellular uptake of acetate, the intracellular triacylglycerol (TAG) content, and acetate-induced lipogenesis gene expression. Acetate activated PI3K-AKT signaling and promoted SP1 translocation from the cytosol into the nucleus, where SP1 bound to the GPR43 promoter and upregulated GPR43 transcription. Moreover, the activation of PI3K-AKT-SP1 by acetate facilitated the trafficking of GPR43 from the cytosol to the plasma membrane. In conclusion, acetate upregulated GPR43 expression and function via PI3K-AKT-SP1 signaling in mammary epithelial cells, thereby increasing milk fat synthesis. These results provide an experimental strategy for improving milk lipid synthesis, which is important to the dairy industry.

更新日期：2023-10-23

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