PI3K/AKT/mTOR通路
蛋白激酶B
磷酸化
甾醇调节元件结合蛋白
信号转导
化学
基因沉默
下调和上调
脂滴
甘油三酯
细胞生物学
生物
内科学
生物化学
内分泌学
基因表达
胆固醇
基因
医学
作者
Yuguang Meng,Chen-Chen Lyu,Yun-Tong He,Hao-Yu Che,Hao Jiang,Jiabao Zhang,Hongyu Tang,Bao Yuan
标识
DOI:10.1021/acs.jafc.3c07812
摘要
Milk fat content is a critical indicator of milk quality. Exploring the key regulatory genes involved in milk fat synthesis is essential for enhancing milk fat content. STF-62247 (STF), a thiazolamide compound, has the potential to bind with ALG5 and upregulate lipid droplets in fat synthesis. However, the effect of STF on the process of milk fat synthesis and whether it acts through ALG5 remains unknown. In this study, the impact of ALG5 on milk fat synthesis and its underlying mechanism were investigated using bovine mammary epithelial cells (BMECs) and mouse models through real-time PCR, western blotting, Oil Red O staining, and triglyceride analysis. Experimental findings revealed a positive correlation between STF and ALG5 with the ability to synthesize milk fat. Silencing ALG5 led to decreased expression of FASN, SREBP1, and PPARγ in BMECs, as well as reduced phosphorylation levels in the PI3K/AKT/mTOR signaling pathway. Moreover, the phosphorylation levels of the PI3K/AKT/mTOR signaling pathway were restored when ALG5 silencing was followed by the addition of STF. These results suggest that STF regulates fatty acid synthesis in BMECs by affecting the PI3K/AKT/mTOR signaling pathway through ALG5. ALG5 is possibly a new factor in milk fat synthesis.
科研通智能强力驱动
Strongly Powered by AbleSci AI