Association of the gut microbiota with type 2 diabetes: Links to disease and remission in the Japanese population

Abstract

Background: Although the gut microbiota is associated with type 2 diabetes (T2D) and its remission in clinical settings, their relationship in the general population remains unclear. This study aimed to investigate the association between the gut microbiota and T2D and its remission in a population-based setting.

Methods: A cross-sectional study was conducted on 1,639 Japanese participants with (n = 106) or without (n = 1,533) T2D. The gut microbiota was compared between the two groups using multivariable-adjusted logistic regression. The relative abundance of the gut microbiota in fecal samples was calculated using 16S ribosomal RNA amplification. The association between the gut microbiota and T2D remission was determined via longitudinal analyses.

Results: Six genera were independently associated with T2D; a higher abundance of Faecalibacterium, Blautia, Roseburia, and Oscillibacter was significantly associated with a lower odds ratio for T2D, whereas a higher abundance of Megasphaera and Lactobacillus was significantly associated with a higher odds ratio for T2D. Of these, only Blautia abundance was significantly increased in the remission group compared with that in the non-remission group. In the remission group, an increase in Blautia abundance was significantly correlated with an increase in adiponectin level and skeletal muscle mass.

Conclusions: Specific gut microbes were significantly associated with T2D and its remission. The gut microbiota may represent a potential area for further exploration in T2D treatment and prevention. However, additional large-scale cohort studies or intervention studies using a probiotic or prebiotic approach are needed to validate these findings.

Keywords: Gut microbiota; Remission; Type 2 diabetes.

Figure 1

Comparison of the gut microbiota between the non‐type 2 diabetes (T2D) and T2D groups. (a) Comparison of α‐diversity (Shannon index) between the non‐T2D and T2D groups. Data are presented as means with 95% confidence intervals (CIs). P‐values were calculated using the Mann–Whitney U test. (b) Comparison of β‐diversity (PCoA plot of Bray–Curtis dissimilarity) between the non‐T2D and T2D groups. P‐values were calculated using permutational multivariate analysis of variance. (c) Comparison of relative microbial abundance using the logarithmic LDA score of effect size between the non‐T2D and the T2D groups. Analysis was performed using α = 0.05 and a threshold of the logarithmic LDA score = 3.0. (d) Association between the gut microbiota and T2D. Data are presented as odds ratios (per one SD) with 95% CI. Logistic regression models were used, with adjustments for age, sex, smoking status, exercise habits, alcohol intake, energy intake, total dietary fiber intake, and visceral fat area. *FDR < 0.05; **FDR < 0.01; ***FDR < 0.001. FDR, false discovery rate; LDA, linear discrimination analysis; PCoA, principal coordinate analysis; OR, odds ratio.

Figure 2

Comparison of changes in the six genera between non‐remission and type 2 diabetes (T2D) remission groups. Data are presented as adjusted means with 95% confidence intervals (CIs). Linear regression models were used, with adjustments for baseline parameters of sex, age, smoking habits, exercise habits, alcohol intake, energy intake, dietary fiber intake, visceral fat area, and abundance of each gut microbe.