Glucose transporter 4 mediates LPS-induced IL-6 production in osteoblasts under high glucose conditions

J Oral Sci. 2020 Sep 26;62(4):423-426. doi: 10.2334/josnusd.20-0010. Epub 2020 Aug 31.

Abstract

Purpose: Diabetes causes hyperglycemic disorders due to insufficient activity of insulin, and it also increases blood glucose level. Recent studies have reported the relationship between diabetes and periodontal disease. Periodontitis is advanced by inflammatory cytokines stimulated with LPS. The purpose of this study was to investigate the effects of hyperglycemia on the expression of inflammatory cytokines induced by LPS in osteoblasts.

Methods: Cells were cultured for 7 and 14 days in the presence or absence of LPS and glucose. The expression mRNA level of IL-6, RANKL and OCN was determined using real-time PCR. The protein expression of IL-6 and RANKL was also measured using ELISA.

Results: LPS and glucose increased the mRNA expression of IL-6, coupled with a decrease in the mRNA expression of OCN, which is associated with IL-6 and glucose. It also increased the protein expression of IL-6 compared to LPS. However, LPS+Glucose did not affect the mRNA and protein expression of RANKL. Furthermore, GLUT4 inhibitor, WZB117, blocked the stimulatory effect of glucose on LPS-induced IL-6 mRNA expression. WZB117 did not affect LPS-reduced OCN mRNA expression.

Conclusion: These results suggest that high glucose levels increase LPS-induced IL-6 expression mediated by GLUT4.

Keywords: GLUT4; LPS; glucose; proinflammatory cytokine.

MeSH terms

  • Glucose
  • Glucose Transport Proteins, Facilitative
  • Glucose Transporter Type 4 / physiology*
  • Interleukin-6* / metabolism
  • Lipopolysaccharides*
  • Osteoblasts / metabolism

Substances

  • Glucose Transport Proteins, Facilitative
  • Glucose Transporter Type 4
  • Interleukin-6
  • Lipopolysaccharides
  • SLC2A4 protein, human
  • Glucose