Thiazolidinedione (pioglitazone) blocks P. gingivalis- and F. nucleatum, but not E. coli, lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) production in adipocytes

M. Yamaguchi, F. Nishimura, H. Naruishi, Yoshihiko Soga, Susumu Kokeguchi, Shogo Takashiba

Research output: Contribution to journalArticle

7 Citations (Scopus)


An elevated level of C-reactive protein (CRP) predicts the future development of coronary heart disease. Periodontitis appears to up-regulate CRP. CRP is produced by hepatocytes in response to interleukin-6 (IL-6). A major source of IL-6 in obese subjects is adipocytes. We hypothesized that lipopolysaccharide (LPS) from periodontal pathogens stimulated adipocytes to produce IL-6, and that the production was suppressed by the drugs targeted against insulin resistance, thiazolidinedione (pioglitazone), since this agent potentially showed an anti-inflammatory effect. Mouse 3T3-L1 adipocytes were stimulated with E. coli, P. gingivalis, and F. nucleatum LPS. The IL-6 concentration in culture supernatants was measured. All LPS stimulated adipocytes to produce IL-6. Although pioglitazone changed adipocyte appearance from large to small, and completely suppressed P. gingivalis and F. nucleatum LPS-induced IL-6 production, E. coli LPS-induced IL-6 production was not efficiently blocked. Thus, pioglitazone completely blocked periodontal-bacteria- derived LPS-induced IL-6 production in adipocytes, a major inducer of CRP.

Original languageEnglish
Pages (from-to)240-244
Number of pages5
JournalJournal of Dental Research
Issue number3
Publication statusPublished - Mar 2005



  • Adipocyte
  • Diabetes
  • Insulin resistance
  • Interleukin-6
  • Thiazolidinedione

ASJC Scopus subject areas

  • Dentistry(all)

Cite this