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Kisspeptin-10 Maintains the Activation of the mTOR Signaling Pathway by Inhibiting SIRT6 to Promote the Synthesis of Milk in Bovine Mammary Epithelial Cells
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2021-04-05 , DOI: 10.1021/acs.jafc.0c07613
Yu Cao 1 , Guiqiu Hu 1 , Qing Zhang 1 , Lijun Ma 1 , Jiaxin Wang 1 , Wen Li 1 , Yusong Ge 1 , Ji Cheng 1 , Zhanqing Yang 1 , Shoupeng Fu 1 , Juxiong Liu 1
Affiliation  

Kisspeptin-10 (Kp-10) is a peptide hormone that regulates normal physiological processes. The mechanism of Kp-10 in milk synthesis is still unclear. Therefore, bovine mammary epithelial cells (BMECs) were used to study the mechanism by which Kp-10 affects milk synthesis in BMECs. The GPR54 inhibitor and SIRT6 overexpression plasmid and siRNA were used to study the mechanism of regulating milk protein and milk fat synthesis by Kp-10. The results showed that 100 nM Kp-10 increased milk synthesis in BMECs. SIRT6 overexpression could significantly reduce the milk protein and milk fat synthesis in BMECs. Moreover, overexpression of SIRT6 reversed the activation of the Kp-10-induced mTOR signaling pathway. Further analysis suggested that SIRT6 might regulate the signal transduction of mTOR at the transcriptional level. These results strongly suggested that Kp-10/GPR54 activated the mTOR signaling pathway by inhibiting SIRT6 expression and then increased the milk synthesis in BMECs.

中文翻译:

Kisspeptin-10通过抑制SIRT6促进牛乳腺上皮细胞中牛奶的合成来维持mTOR信号通路的激活。

Kisspeptin-10(Kp-10)是一种调节正常生理过程的肽激素。Kp-10在牛奶合成中的机制仍不清楚。因此,牛乳腺上皮细胞(BMECs)用于研究Kp-10影响BMECs牛奶合成的机制。使用GPR54抑制剂和SIRT6过表达质粒以及siRNA来研究Kp-10调节乳蛋白和乳脂合成的机制。结果表明,100 nM Kp-10增加了BMEC中的牛奶合成。SIRT6的过表达可显着降低BMEC中的乳蛋白和乳脂合成。此外,SIRT6的过表达逆转了Kp-10-诱导的mTOR信号通路的激活。进一步的分析表明,SIRT6可能在转录水平上调节mTOR的信号转导。
更新日期:2021-04-14
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