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Subgingival Microbiota and Longitudinal Glucose Change: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS).

ABSTRACT: Microbial communities along mucosal surfaces throughout the digestive tract are hypothesized as risk factors for impaired glucose regulation and the development of clinical cardiometabolic disease. We investigated whether baseline measures of subgingival microbiota predicted fasting plasma glucose (FPG) longitudinally. The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 230 diabetes-free adults (77% female) aged 20 to 55 y (mean ± SD, 34 ± 10 y) from whom baseline subgingival plaque and longitudinal FPG were measured. DNA was extracted from subgingival plaque, and V3 to V4 regions of the 16S rRNA gene were sequenced. FPG was measured at baseline and again at 2 y; glucose change was defined as follow-up minus baseline. Multivariable linear models regressed 2-y glucose change onto baseline measures of community diversity and abundances of 369 individual taxa. A microbial dysbiosis index (MDI) summarizing top individual taxa associated with glucose change was calculated and used in regression models. Models were adjusted for age, sex, race/ethnicity, education, smoking status, body mass index, and baseline glucose levels. Statistical significance was based on the false discovery rate (FDR; <0.05) or a Bonferroni-corrected P value of 1 × 10^-4, derived from the initial 369 hypothesis tests for specific taxa. Mean 2-y FPG change was 1.5 ± 8 mg/dL. Baseline levels of 9 taxa predicted FPG change (all FDR <0.05), among which Stomatobaculum sp oral taxon 097 and Atopobium spp predicted greater FPG change, while Leptotrichia sp oral taxon 498 predicted lesser FPG change (all 3 P values, Bonferroni significant). The MDI explained 6% of variation in longitudinal glucose change (P < 0.001), and baseline glucose levels explained 10% of variation (P < 0.0001). FPG change values ± SE in the third versus first tertile of the MDI were 4.5 ± 0.9 versus 1.6 ± 0.9 (P < 1 × 10^-4). Subgingival microbiota predict 2-y glucose change among diabetes-free men and women.

SUBMITTER: Demmer RT

PROVIDER: S-EPMC6873283 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Subgingival Microbiota and Longitudinal Glucose Change: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS).

Demmer R T RT Trinh P P Rosenbaum M M Li G G LeDuc C C Leibel R R González A A Knight R R Paster B B Colombo P C PC Desvarieux M M Papapanou P N PN Jacobs D R DR

Journal of dental research 20191017 13

Microbial communities along mucosal surfaces throughout the digestive tract are hypothesized as risk factors for impaired glucose regulation and the development of clinical cardiometabolic disease. We investigated whether baseline measures of subgingival microbiota predicted fasting plasma glucose (FPG) longitudinally. The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 230 diabetes-free adults (77% female) aged 20 to 55 y (mean ± SD, 34 ± 10 y) from whom bas ...[more]

PMID: 31623509

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Project description:Periodontitis and type 2 diabetes mellitus are known to be associated. The relationship between periodontal microbiota and early diabetes risk has not been studied. We investigated the association between periodontal bacteria and prediabetes prevalence among diabetes-free adults. ORIGINS (the Oral Infections, Glucose Intolerance and Insulin Resistance Study) cross sectionally enrolled 300 diabetes-free adults aged 20 to 55 y (mean ± SD, 34 ± 10 y; 77% female). Prediabetes was defined as follows: 1) hemoglobin A1c values ranging from 5.7% to 6.4% or 2) fasting plasma glucose ranging from 100 to 125 mg/dL. In 1,188 subgingival plaque samples, 11 bacterial species were assessed at baseline, including Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Actinomyces naeslundii. Full-mouth clinical periodontal examinations were performed, and participants were defined as having no/mild periodontitis vs. moderate/severe periodontitis per the definition of the Centers for Disease Control and Prevention / American Academy of Periodontology. Modified Poisson regression evaluated prediabetes prevalence across bacterial tertiles. Prevalence ratios and 95% confidence intervals for third vs. first tertiles are presented. All analyses were adjusted for cardiometabolic risk factors. All results presented currently arise from the baseline cross section. Prediabetes prevalence was 18%, and 58% of participants had moderate/severe periodontitis. Prevalence ratios (95% confidence intervals) summarizing associations between bacterial levels and prediabetes were as follows: A. actinomycetemcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola, 1.99 (0.992, 4.00), P = 0.052; T. forsythia, 1.95 (1.0, 3.84), P = 0.05; A. naeslundii, 0.46 (0.25, 0.85), P = 0.01. The prevalence ratio for prediabetes among participants with moderate/severe vs. no/mild periodontitis was 1.47 (0.78, 2.74), P = 0.23. Higher colonization levels of specific periodontal microbiota are associated with higher prediabetes prevalence among diabetes-free adults.

Project description:ImportancePeripheral glucose homeostasis has been implicated in the pathogenesis of Alzheimer disease (AD). The relationship among diabetes mellitus, insulin, and AD is an important area of investigation. However, whether cognitive impairment seen in those with diabetes is mediated by excess pathological features of AD or other related abnormalities, such as vascular disease, remains unclear.ObjectiveTo investigate the association between serial measures of glucose intolerance and insulin resistance and in vivo brain β-amyloid burden, measured with carbon 11–labeled Pittsburgh Compound B (11C-PiB), and AD pathology at autopsy.DesignScores calculated from the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) and Braak criteria were correlated with measures of hyperglycemia, hyperinsulinemia, glucose intolerance, and insulin resistance in 197 participants who underwent autopsy after death and who had undergone 2 or more oral glucose tolerance tests (OGTT) using grouped analyses and a continuous mixed-models analysis. The same measures of glucose intolerance and insulin resistance were also correlated with brain 11C-PiB retention in an additional 53 living subjects from the Baltimore Longitudinal Study of Aging neuroimaging study.SettingProspective, serially assessed cohort of community-dwelling subjects.ParticipantsCohort 1 consisted of 197 participants enrolled in the Baltimore Longitudinal Study of Aging who had 2 or more OGTTs during life and a complete brain autopsy after death. Cohort 2 consisted of 53 living subjects who had 2 or more OGTTs and underwent brain 11C-PiB positron emission tomography.ExposuresAutopsy and 11C-PiB positron emission tomography.Main outcomes and measuresThe correlation of brain markers of AD, including CERAD score, Braak score, and 11C-PiB retention, with serum markers of glucose homeostasis using grouped and continuous mixed-models analyses.ResultsWe found no significant correlations between measures of brain AD pathology or 11C-PiB β-amyloid load and glucose intolerance or insulin resistance in subjects who had a mean (SD) of 6.4 (3.2) OGTTs during 22.1 (8.0) years of follow-up. Thirty subjects with frank diabetes mellitus who received medications also had AD pathology scores that were similar to those of the cohort as a whole.Conclusions and relevanceIn this prospective cohort with multiple assessments of glucose intolerance and insulin resistance, measures of glucose and insulin homeostasis are not associated with AD pathology and likely play little role in AD pathogenesis. Long-term therapeutic trials are important to elucidate this issue.

Project description:BackgroundTo assess the impact of changes in different glucose tolerance states on risk of incident cardiovascular disease (CVD)/coronary heart disease (CHD).MethodsA total of 4094 Iranians (43.9% men) aged ≥ 30 years, without diabetes and CVD at enrolment were included. The following categories were defined both at baseline visit and 3 years later (second visit): normal fasting glucose (NFG), normal glucose tolerance (NGT), NFG and NGT (NFG/NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and IFG and/or IGT (IFG/IGT). Changes in the categories, i.e. regression to normoglycemia, remaining in previous status and progression to diabetes were assessed. We used Cox's proportional hazard models adjusted for traditional risk factors and their changes, to estimate the hazard ratio (HR) with 95% confidence interval (CI) of different changing categories for incident CVD/CHD.ResultsDuring a median follow-up of 12.42 years, 428 subjects (men = 265) experienced CVD. Considering persistent NFG/NGT as reference, participants who shifted from NFG/NGT to IFG/IGT showed a lower hazard of CVD in the fully adjusted model, HR 0.72 [95% CI 0.52-0.996, P = 0.048]. Moreover, subjects who shifted from IFG, IGT and IFG/IGT to diabetes had an increased risk of CVD/CHD. The risk however, was only statistically significant for those with IFG/IGT, 1.61 [(1.03-2.51), P = 0.04] for CVD and 1.75 [(1.10-2.78), P = 0.02] for CHD; considering IFG/IGT at both visits as reference. Furthermore, those who regressed from IFG/IGT to normoglycemia were at the same risk as those remained in IFG/IGT state, 1.12 [(0.79-1.60), P = 0.52] for CVD and 1.04 [(0.70-1.53), P = 0.85] for CHD. Among a subgroup of population with insulin data (n = 803) those with insulin resistance (IR) that converted to diabetes showed a higher risk for CVD, 3.68 [(1.49-9.06), P = 0.01] and CHD, 2.76 [(1.00-7.60), P = 0.05] events in the fully adjusted model.ConclusionsAmong participants with IFG, IGT or IFG/IGT at baseline, only those who developed diabetes had a higher risk of developing CVD/CHD. Persistent IFG/IGT was not associated with higher risk, compared with those reverted to normoglycemia. Moreover, subjects who converted from NFG/NGT to incident IFG/IGT showed a signal for lower risk of CVD/CHD.

Dataset Information

Subgingival Microbiota and Longitudinal Glucose Change: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS).

Publications

Subgingival Microbiota and Longitudinal Glucose Change: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS).

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