title: Periodontitis as a novel contributor of adipose tissue inflammation promotes insulin resistance in a rat model.
abstract: BACKGROUND
  Recent studies have indicated that the chronic low-grade inflammation induced by periodontitis is related to obesity and type 2 diabetes mellitus. The purpose of this study is to investigate the effects of periodontitis on obesity-related adipose tissue inflammation and subsequent systemic insulin resistance in a rat model.
  
  
  METHODS
  Thirty-two rats were divided into four groups of eight: 1) obese rats with periodontitis (combination group); 2) obese rats without periodontitis (obesity group); 3) normal rats with periodontitis (periodontitis group); and 4) normal rats without periodontitis (control group). Monosodium glutamate was used to induce obesity during the early postnatal period. Periodontitis was induced by ligatures for 8 weeks. Morphologic features of white adipose tissue (WAT) and islets were observed, and fasting plasma glucose and insulin concentrations and homeostasis model assessment for insulin (HOMA-IR) were measured at 5 months. Differences among groups were compared with the Fisher post hoc least significant difference test.
  
  
  RESULTS
  A slight increase of stromal vascular fractions (SVFs) and macrophage infiltration in the WAT of the periodontitis group was observed. Significant proliferation of SVFs and macrophage infiltration were induced in the combination group. HOMA-IR scores in the combination and periodontitis groups were higher than in the obesity and control groups, respectively. The disturbance of islet architecture was consistent with a high HOMA-IR score in the combination group.
  
  
  CONCLUSIONS
  Periodontitis induced initial stages of WAT inflammation and acted as a contributing factor to exacerbate proinflammatory phenotype of WAT and promote the development of insulin resistance in the obese rat model.
authors.affiliation: Department of Periodontology, Guangdong Provincial Stomatological Hospital, Southern Medical University, Guangzhou, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Su
authors.forename: Dan
authors.initials: D
authors.lastname: Wang
authors.forename: Dongying
authors.initials: D
authors.lastname: Xuan
authors.forename: Jia
authors.initials: J
authors.lastname: Ni
authors.forename: Shigao
authors.initials: S
authors.lastname: Luo
authors.forename: Baoyi
authors.initials: B
authors.lastname: Xie
authors.forename: Jincai
authors.initials: J
authors.lastname: Zhang
mesh_terms: D017667:Adipocytes / Q000473:pathology; D052436:Adipose Tissue, White / Q000473:pathology*; D016301:Alveolar Bone Loss / Q000150:complications; D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001786:Blood Glucose / Q000032:analysis; D002452:Cell Count; D048430:Cell Shape; D004195:Disease Models, Animal; D005215:Fasting; D005421:Flavoring Agents / Q000009:adverse effects; D021621:Imaging, Three-Dimensional / Q000379:methods; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008264:Macrophages / Q000473:pathology; D008297:Male; D009765:Obesity / Q000150:complications*; D010518:Periodontitis / Q000150:complications*; D010641:Phenotype; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012970:Sodium Glutamate / Q000009:adverse effects; D017154:Stromal Cells / Q000473:pathology; D013997:Time Factors; D055114:X-Ray Microtomography / Q000379:methods; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001786:Blood Glucose; D005421:Flavoring Agents; D007328:Insulin; D018950:Lipopolysaccharide Receptors; D012970:Sodium Glutamate; C539355:CD68 protein, rat; D000097382:CD68 Molecule