Diet Supplementation with NUTRIOSE, a Resistant Dextrin, Increases the Abundance of Parabacteroides distasonis in the Human Gut

Abstract

Scope: An imbalance of the gut microbiota ("dysbiosis") is associated with numerous chronic diseases, and its modulation is a promising novel therapeutic approach. Dietary supplementation with soluble fiber is one of several proposed modulation strategies. This study aims at confirming the impact of the resistant dextrin NUTRIOSE (RD), a soluble fiber with demonstrated beneficial health effects, on the gut microbiota of healthy individuals.

Methods and results: Fifty healthy women are enrolled and supplemented daily with either RD (n = 24) or a control product (n = 26) during 6 weeks. Characterization of the fecal metagenome with shotgun sequencing reveals that RD intake dramatically increases the abundance of the commensal bacterium Parabacteroides distasonis. Furthermore, presence in metagenomes of accessory genes from P. distasonis, coding for susCD (a starch-binding membrane protein complex) is associated with a greater increase of the species. This suggests that response to RD might be strain-dependent.

Conclusion: Supplementation with RD can be used to specifically increase P. distasonis in gut microbiota of healthy women. The magnitude of the response may be associated with fiber-metabolizing capabilities of strains carried by subjects. Further research will seek to confirm that P. distasonis directly modulates the clinical effects observed in other studies.

Keywords: Parabacteroides distasonis; gut microbiota; resistant dextrin; shotgun metagenomics; soluble fiber.

Figure 1

Clinical trial. A) Study design. Stool samples are collected and analyzed at baseline and D42. B) Clinical trial flowchart.

Figure 2

Evolution in gut microbiota global composition between RD and CP. A) Comparison of MGS richness between baseline and D42 in the RD group or in the CP group. P‐values associated with paired Wilcoxon test are displayed. P‐value associated with the test for nonparametric longitudinal data (nparld, see Methods) is displayed at the top. B) Comparison of intraindividuals Bray–Curtis dissimilarity between the RD and the CP group. P‐value associated with Wilcoxon test is displayed. CP indicates control product; MGS, MetaGenomic species; RD, resistant dextrin.

Figure 3

Metagenomic features altered by RD intake. A) Evolution of the relative abundance of Parabacteroides distasonis in the RD and the CP group. P‐values associated with paired Wilcoxon test are displayed. Q‐value associated with the test for nonparametric longitudinal data (nparld, see Methods) is displayed at the top. B) Evolution if the six CAZymes impacted by RD intake. Q‐value associated with the test for nonparametric longitudinal data (nparld, see Methods) is displayed for each CAZymes. CP indicates control product; RD, resistant dextrin; rel. ab., relative abundance.

Figure 4

Focus on Parabacteroides distasonis. A) Relation between P. distasonis log‐fold change and intraindividuals Bray–Curtis dissimilarity, considering only individuals from the RD group carrying P. distasonis (n = 21). Spearman's coefficient along with the associated p‐value are displayed. B) Barcode of P. distasonis in the RD group (left) or in the CP group (right), at baseline (top) or at D42 (bottom). The 50 “tracer” genes are in rows, abundance is indicated by color gradient (white, not detected; red, most abundant); individuals, ordered by increasing MGS richness, are in columns. The lowest bar gives the log‐fold change between baseline and D42 associated with each individual (i.e., each column). C) Difference in P. distasonis log‐fold change when comparing individuals from the RD group whose P. distasonis strain carries a specific gene annotated as SusD (n = 10) with individuals whose strain does not have this gene (n = 11). CP indicates control product; log2FC, log‐fold change; MGS, MetaGenomic species; RD, resistant dextrin.