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J Clin Periodontol. 2016 Dec 15. doi: 10.1111/jcpe.12664. [Epub ahead of print]

The subgingival microbiome, systemic inflammation and insulin resistance: The Oral Infections, Glucose Intolerance and Insulin Resistance Study.

Author information

  • 1Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
  • 2Division of Molecular Genetics, Departments of Pediatrics and Medicine, Columbia University, New York, NY, USA.
  • 3Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada.
  • 4Department of Molecular Genetics, The Forsyth Institute, Cambridge, MA, USA.
  • 5Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, MA, USA.
  • 6Centre de recherche Epidémiologies et Biostatistique, INSERM U1153 Equipe: Méthodes en évaluation thérapeutique des maladies chroniques, Paris, France.
  • 7Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA.
  • 8Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY, USA.

Abstract

BACKGROUND:

Inflammation might link microbial exposures to insulin resistance. We investigated the cross-sectional association between periodontal microbiota, inflammation and insulin resistance.

METHODS:

The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 152 diabetes-free adults (77% female) aged 20-55 years (mean = 34 ± 10). Three hundred and four subgingival plaque samples were analysed using the Human Oral Microbe Identification Microarray to measure the relative abundances of 379 taxa. C-reactive protein, interleukin-6, tumour necrosis factor-α and adiponectin were assessed from venous blood and their z-scores were summed to create an inflammatory score (IS). Insulin resistance was defined via the HOMA-IR. Associations between the microbiota and both inflammation and HOMA-IR were explored using multivariable linear regressions; mediation analyses assessed the proportion of the association explained by inflammation.

RESULTS:

The IS was inversely associated with Actinobacteria and Proteobacteria and positively associated with Firmicutes and TM7 (p-values < 0.05). Proteobacteria levels were associated with insulin resistance (p < 0.05). Inflammation explained 30-98% of the observed associations between levels of Actinobacteria, Proteobacteria or Firmicutes and insulin resistance (p-values < 0.05). Eighteen individual taxa were associated with inflammation (p < 0.05) and 22 with insulin resistance (p < 0.05). No findings for individual taxa met Bonferroni-adjusted statistical significance.

CONCLUSION:

Bacterial measures were related to inflammation and insulin resistance among diabetes-free adults.

KEYWORDS:

C-reactive protein; adiponectin; diabetes; inflammation; insulin resistance; interleukin-6; microbiome; microbiota; periodontal; tumour necrosis factor-α

PMID:
27978598
DOI:
10.1111/jcpe.12664
[PubMed - as supplied by publisher]
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