title: Experimental periodontitis induces gene expression of proinflammatory cytokines in liver and white adipose tissues in obesity.
abstract: BACKGROUND
  Recent studies indicated that periodontitis induces systemic low-grade inflammation. The increase in systemic low-grade inflammation induced by periodontitis may alter the effects of obesity on the production of inflammatory molecules, including C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-alpha), in the liver and white adipose tissue (WAT). The purpose of the present study is to investigate the effects of periodontitis on the expression of proinflammatory cytokines in the liver and WAT in obese Zucker rats.
  
  
  METHODS
  Obese Zucker rats and their lean litter mates were divided into four groups of six rats each: lean Zucker rats without periodontitis (control group), lean Zucker rats with periodontitis (periodontitis group), obese Zucker rats without periodontitis (obesity group), and obese Zucker rats with periodontitis (combination group). Periodontitis was ligature induced for 4 weeks in the periodontitis and combination groups, whereas the other groups were left unligated.
  
  
  RESULTS
  At 4 weeks, the gene expression for CRP, IL-6, and TNF-alpha in the liver and CRP and IL-6 in the WAT of combination groups was significantly higher than in each of the three groups. Serum TNF-alpha in the periodontitis and obesity groups was significantly higher than in the control group. Serum CRP and TNF-alpha in the combination group was significantly higher than in each of the three groups.
  
  
  CONCLUSIONS
  Systemic low-grade inflammation after experimental periodontitis was associated with increased gene expression for hepatic levels of TNF-alpha and CRP and adipose tissue levels of IL-6 and CRP in the obese-rat model.
authors.affiliation: Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Endo
authors.forename: Takaaki
authors.initials: T
authors.lastname: Tomofuji
authors.forename: Daisuke
authors.initials: D
authors.lastname: Ekuni
authors.forename: Koichiro
authors.initials: K
authors.lastname: Irie
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Azuma
authors.forename: Naofumi
authors.initials: N
authors.lastname: Tamaki
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Manabu
authors.initials: M
authors.lastname: Morita
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D002097:C-Reactive Protein / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D015870:Gene Expression; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D008026:Ligation; D008099:Liver / Q000378:metabolism*; D008297:Male; D009765:Obesity / Q000150:complications / Q000235:genetics / Q000378:metabolism; D010518:Periodontitis / Q000150:complications / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D011897:Random Allocation; D051381:Rats; D011924:Rats, Zucker; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D015854:Up-Regulation
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein