Study on the mechanism of SAR1B in sodium acetate promoting milk fat synthesis.

Abstract

Acetate can promote milk fat synthesis in dairy cow mammary epithelial cells (BMECs). In this study, gene function analysis was used to explore the role of Ras family secretion-related GTP binding protein 1B (SAR1B) in milk fat synthesis of BMECs and its role and molecular mechanism in acetate-promoted milk fat synthesis. We found that the synthesis of lipid droplets and triglycerides was inhibited, and the expression levels of key genes and proteins in milk fat synthesis such as FASN and ACC were decreased in SAR1B knockout, which was reversed by overexpression of SAR1B. Addition of sodium acetate in BMECs can promote the expression of SAR1B, and SAR1B plays an important role in the synthesis of milk fat promoted by sodium acetate. We further investigated the underlying mechanism of SAR1B upregulation by sodium acetate, and found that sodium acetate could affect SAR1B expression through the positive regulation of SAR1B gene promoter activity by C/EBPβ and PPARγ. In conclusion, the results suggest that SAR1B can promote milk fat synthesis in BMECs, while C/EBPβ and PPARγ play important roles in sodium acetate to promote the expression of SAR1B.