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IL-1β directly inhibits milk lipid production in lactating mammary epithelial cells concurrently with enlargement of cytoplasmic lipid droplets

Journal Article · · Experimental Cell Research
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  1. Laboratory of Cell and Tissue Biology, Research Faculty of Agriculture, Hokkaido University, North 9, West 9, Sapporo, 060-8589 (Japan)
Highlights: • IL-1β inhibits milk lipid production concurrently with enlargement of lipid droplets. • IL-1β, IL-6, and TNF-α affect milk lipid production in different manners. • IL-1β rapidly induced activation of STAT3 concurrently with inactivation of STAT5. • IL-1β activates the mRNA expression of IL-6 and TNF-α in mammary epithelial cells. 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-1β, IL-6, and TNF-α 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-α, IL-1β, and IL-6 differentially affected lipid production and secretion in lactating MECs. In particular, IL-1β treatment significantly reduced amounts of secreted triglycerides by 97% compared with the control concurrently with enlargement of cytoplasmic lipid droplets in MECs. IL-1β 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-1β inactivated STAT5 and glucocorticoid signaling to induce milk production in MECs, whereas STAT3 and NFκB signaling was activated. IL-1β induced mRNA expression of IL-6 and TNF-α in MECs. Therefore, we suggest that IL-1β is a key inhibitor of lipid production and secretion in lactating MECs.
OSTI ID:
23082649
Journal Information:
Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 2 Vol. 370; ISSN 0014-4827; ISSN ECREAL
Country of Publication:
United States
Language:
English