Abstract
Periodontal infection induces systemic inflammation; therefore, aggravating diabetes. Orally administered periodontal pathogens may directly alter the gut microbiota. We orally treated obese db/db diabetes mice using Porphyromonas gingivalis (Pg). We screened for Pg-specific peptides in the intestinal fecal specimens and examined whether Pg localization influenced the intestinal microbiota profile, in turn altering the levels of the gut metabolites. We evaluated whether the deterioration in fasting hyperglycemia was related to the changes in the intrahepatic glucose metabolism, using proteome and metabolome analyses. Oral Pg treatment aggravated both fasting and postprandial hyperglycemia (P < 0.05), with a significant (P < 0.01) increase in dental alveolar bone resorption. Pg-specific peptides were identified in fecal specimens following oral Pg treatment. The intestinal Pg profoundly altered the gut microbiome profiles at the phylum, family, and genus levels; Prevotella exhibited the largest increase in abundance. In addition, Pg-treatment significantly altered intestinal metabolite levels. Fasting hyperglycemia was associated with the increase in the levels of gluconeogenesis-related enzymes and metabolites without changes in the expression of proinflammatory cytokines and insulin resistance. Oral Pg administration induced gut microbiota changes, leading to entero-hepatic metabolic derangements, thus aggravating hyperglycemia in an obese type 2 diabetes mouse model.
Highlights
Periodontal infection induces systemic inflammation; aggravating diabetes
Blood glucose levels under ad libitum feeding in Porphyromonas gingivalis (Pg)-administered mice was significantly (P < 0.05) higher than that in control mice after 4 weeks of oral Pg treatment without any differences in both food intake, body wight and blood glucose at ad libitum feeding during 4-week period between 2 groups (Table 1)
Specific Pg-derived peptides were present in the fecal specimens from db/db diabetic mice after 30 days following oral Pg-administration
Summary
Periodontal infection induces systemic inflammation; aggravating diabetes. Advanced stages of periodontitis may further impair glycemic control in diabetic p atients[13] The mechanisms connecting these conditions has not been elucidated; it is speculated that local infection by oral pathogens, and the release of inflammatory cytokines into blood vessels, could explain the systemic effects of periodontal d isease[7,8,9,14]. Recent studies have proposed that the dissemination of periodontal pathogens into the intestinal tract may induce systemic inflammation, metabolic changes, and fatty liver disease in non-diabetic mice models[15,16]. Clarifying this requires identification of orally administered periodontal bacteria in fecal specimens. Oral bacteria mixed with saliva and food can survive in the acidic stomach environment, and subsequently be transmitted to the intestinal tract with food[17]
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