β-1,4-Galactan suppresses lipid synthesis in sebaceous gland cells via TLR4

Abstract

Summary Sebum is a lipid mixture secreted from sebaceous glands of the skin. The excessive secretion of sebum causes acne vulgaris and seborrheic dermatitis, while its deficiency causes xerosis. Therefore, the appropriate control of sebum secretion is crucially important to keep the skin healthy. In the present study, we evaluated the effects of naturally occurring polysaccharides on lipid biosynthesis in hamster sebaceous gland cells. Among the tested polysaccharides, β-1,4-galactan, the main chain of type I arabinogalactan, most potently suppressed lipid synthesis in the sebaceous gland cells as analyzed by oil red O staining. Toll-like receptor (TLR)4 inhibitors counteracted this suppressive effect and lipopolysaccharide, a TLR4 ligand, mimicked this effect, suggesting the involvement of the TLR4 signaling pathway. In the cells β-1,4-galactan significantly decreased mRNA levels of lipogenesis-related transcription factors (peroxisome proliferator-activated receptor γ and sterol regulatory element-binding protein 1) and enzymes (acetyl-CoA carboxylase and fatty acid synthase) as well as the glucose transporter GLUT4. Furthermore, β-1,4-galactan increased the production of lactic acid serving as a natural moisturizing factor and enhanced the proliferation of sebaceous gland cells. These results suggest potential of β-1,4-galactan as a material with therapeutic and cosmetic values for the skin.