Regulation of peroxisome proliferator-activated receptor gamma on milk fat synthesis in dairy cow mammary epithelial cells

Peroxisome proliferator-activated receptor gamma (PPAR gamma) participates in lipogenesis in rats, goats, and humans. However, the exact mechanism of PPAR gamma regulation on milk fat synthesis in dairy cow mammary epithelial cells (DCMECs) remains largely unexplored. The aim of this study was to investigate the role of PPAR gamma regarding milk fat synthesis in DCMECs and to ascertain whether milk fat precursor acetic acid and palmitic acid could interact with PPAR gamma signaling to regulate milk fat synthesis. For this study, we examined the effects of PPAR gamma overexpression and gene silencing on cell growth, triacylglycerol synthesis, and the messenger RNA (mRNA) and protein expression levels of genes involved in milk fat synthesis in DCMECs. In addition, we investigated the influences of acetic acid and palmitic acid on the mRNA and protein levels of milk lipogenic genes and triacylglycerol synthesis in DCMECs transfected with PPAR gamma small interfering RNA (siRNA) and PPAR gamma expression vector. The results showed that when PPAR gamma was silenced, cell viability, proliferation, and triacylglycerol secretion were obviously reduced. Gene silencing of PPAR gamma significantly downregulated the expression levels of milk fat synthesis-related genes in DCMECs. PPAR gamma overexpression improved cell viability, proliferation, and triacylglycerol secretion. The expression levels of milk lipogenic genes were significantly increased when PPAR gamma was overexpressed. Acetic acid and palmitic acid could markedly improve triacylglycerol synthesis and upregulate the expression levels of PPAR gamma and other lipogenic genes in DCMECs. These results suggest that PPAR gamma is a positive regulator of milk fat synthesis in DCMECs and that acetic acid and palmitic acid could partly regulate milk fat synthesis in DCMECs via PPAR gamma signaling.