Insulin-Like Growth Factor-1 Increases the Expression of Inflammatory Biomarkers and Sebum Production in Cultured Sebocytes

• Published in: Annals of dermatology 2017, 29(1), , pp.20-25
• Main Authors: Kim, Hyojin, Moon, Sun Young, Sohn, Mi Yeung, Lee, Weon Ju
• Format: Article
• Language: English
• Subjects: Original; 피부과학
• ISSN: 1013-9087; 2005-3894
• DOI: 10.5021/ad.2017.29.1.20

Acne vulgaris has been linked to the Western diet. Hyperglycemic diet increases insulin and insulin-like growth factor (IGF)-1. Deeper insights into IGF-1-mediated signal pathway are critical importance to understand the impact of Western diet. We investigated the effect of IGF-1 on the expression of inflammatory biomarkers and sebum production in cultured sebocytes. Polymerase chain reaction and enzyme-linked immunosorbent assay were performed to measure changes in the expression of inflammatory biomarkers including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), IGF1R, IGFBP2, sterol response element-binding protein (SREBP), and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PI3KCA) after the treatment of cultured sebocytes with 10 M or 10 M IGF-1. Sebum production was evaluated after the treatment of cultured sebocytes with 10 M or 10 M IGF-1 using lipid analysis. The expression levels of IL-1β, IL-6, IL-8, and TNF-α in cultured sebocytes after treatment with 10 M or 10 M IGF-1 were increased. Increased gene expression levels of NF-κB in cultured sebocytes were also shown after 10 M or 10 M IGF-1 treatments. Gene expression of these inflammatory biomarkers was decreased after 10 M or 10 M IGF-1 treatment in the presence of 100 nM NF-κB inhibitor. Treatment with 10 M or 10 M IGF-1 increased the gene expression levels of IGF1R, IGFBP2, SREBP and PI3KCA in cultured sebocytes. Sebum production from cultured sebocytes treated with 10 M or 10 M IGF-1 was also increased. It is suggestive that IGF-1 might be involved in the pathogenesis of acne by increasing both expression of inflammatory biomarkers and also sebum production in sebocytes.