| First Author | Matsunaga K | Year | 2018 |
| Journal | Exp Cell Res | Volume | 370 |
| Issue | 2 | Pages | 365-372 |
| PubMed ID | 29966663 | Mgi Jnum | J:268537 |
| Mgi Id | MGI:6271260 | Doi | 10.1016/j.yexcr.2018.06.038 |
| Citation | Matsunaga K, et al. (2018) IL-1beta directly inhibits milk lipid production in lactating mammary epithelial cells concurrently with enlargement of cytoplasmic lipid droplets. Exp Cell Res 370(2):365-372 |
| abstractText | Mammary epithelial cells (MECs) in lactating mammary glands produce milk lipid, which provides a large percentage of calories and bioactive lipids for appropriate infant growth. However, secreted milk lipid is often reduced concurrently with increases in IL-1beta, IL-6, and TNF-alpha in mammary glands with mastitis. In this study, we investigated whether those cytokines directly influenced lipid production and secretion. A lactating MEC culture model with high lipid production ability was prepared by culture with oleic acid. TNF-alpha, IL-1beta, and IL-6 differentially affected lipid production and secretion in lactating MECs. In particular, IL-1beta treatment significantly reduced amounts of secreted triglycerides by 97% compared with the control concurrently with enlargement of cytoplasmic lipid droplets in MECs. IL-1beta also decreased mRNA expression of Fabp3 and Srebp1 and the amount of aquaporin 3, GLUT-1 and adipophilin in the milk lipid production pathway. Furthermore, IL-1beta inactivated STAT5 and glucocorticoid signaling to induce milk production in MECs, whereas STAT3 and NFkappaB signaling was activated. IL-1beta induced mRNA expression of IL-6 and TNF-alpha in MECs. Therefore, we suggest that IL-1beta is a key inhibitor of lipid production and secretion in lactating MECs. |
