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. 2019 Apr 4;8(4):451.
doi: 10.3390/jcm8040451.

H. pylori Eradication Treatment Alters Gut Microbiota and GLP-1 Secretion in Humans

Affiliations

H. pylori Eradication Treatment Alters Gut Microbiota and GLP-1 Secretion in Humans

Isabel Cornejo-Pareja et al. J Clin Med. .

Abstract

Changes in the intestinal microbial community and some metabolic disturbances, including obesity and type2 diabetes, are related. Glucagon-like peptide-1 (GLP-1) regulates glucose homeostasis. Microbiota have been linked to incretin secretion. Antibiotic use causes changes in microbial diversity and composition. Our aim was to evaluate the relationship between microbiota changes and GLP-1 secretion. A prospective case-control study with a Helicobacter pylori-positive patient model involving subjects under eradication therapy (omeprazole, clarithromycin, and amoxicillin). Forty patients with H. pylori infection and 20 matched participants, but negative for H. pylori antigen. Patients were evaluated before and two months after treatment. We analyzed anthropometric measurements, carbohydrate metabolism, lipid profile, and C-reactive protein. Gut microbiota composition was analyzed through 16S rRNA amplicon sequencing (IlluminaMiSeq). Eradication treatment for H. pylori decreased bacterial richness (Chao1, p = 0.041). Changes in gut microbiota profiles were observed at phylum, family, genus and species levels. GLP-1 secretion and variables of carbohydrate metabolism were improved. Correlations were seen between GLP-1 changes and variations within microbial community abundances, specifically Bifidobacterium adolescentis, the Lachnobacterium genus, and Coriobacteriaceae family. A conventional treatment to eradicate H. pylori could improve carbohydrate metabolism possibly in relation with an increase in GLP-1 secretion. GLP-1 secretion may be related to alterations in intestinal microbiota, specifically Lachnobacterium, B. adolescentis and Coriobacteriaceae.

Keywords: GLP-1 secretion; H. pylori; antibiotic; gut microbiota.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Changes in Glucagon-like peptide-1 (GLP-1) levels after antibiotic therapy compared to the control group. GLP-1 levels in H. pylori-infected patients at baseline and after 75g-OGTT and after 2 months of post-antibiotic treatment compared to the control group. Student’s t-test for paired samples and Student’s t-test between independent samples were used to compare the group of H. pylori-infected patients before and after antibiotic treatment, and control group, respectively. Equal letter means differences between groups. a: differences between H. pylori-infected individuals before and after antibiotic treatment, p < 0.05. b: differences between H. pylori-infected patients and the control group, p < 0.05. c: differences in patients undergoing antibiotic therapy compared to the control group, p < 0.05.
Figure 2
Figure 2
Estimation of diversity in control subjects and H. pylori-infected patients after antibiotic treatment. (a) Richness and diversity indices among different groups were compared. Wilcoxon test was used to compare the group of H. pylori-infected patients before and after antibiotic treatment. Equal letters indicate statistical differences between those groups. a: differences between H. pylori-infected patients before and after antibiotic treatment, p < 0.05. b: differences between H. pylori-infected patients compared to the control group, p < 0.05. c: differences between patients’ post-antibiotic treatment versus control group, p < 0.05. All values are means ± standard error of the mean. (b) Clustering of gut microbiota populations according to the study groups by principal coordinate analysis (PCoA) using the Bray–Curtis dissimilarity. No statistical differences were observed between groups. Orange squares belong to the control subject group; blue triangles to patients before treatment; and red dots to patients after treatment.
Figure 3
Figure 3
Predicted functional composition of metagenomes based on 16S rRNA gene sequencing data of H. pylori infected patients and after the eradication therapy and healthy control subjects. Heatmap shows the differentially abundant Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways identified in the three study groups (FDR-ajusted-P ≤ 0.05).
Figure 4
Figure 4
Correlation between changes in GLP-1 levels at minute 60 and the AUC for GLP-1 with percentage change in microbial community after antibiotic treatment: (a) with Lachnobacterium percentage change; (b) with Bifidobacterium adolescentis percentage change; and (c) with Coriobacteriaceae percentage change.
Figure 5
Figure 5
Microbiota and GLP-1 secretion. The use of conventional antibiotic treatment generates modifications in the intestinal microbiota. In this study, these changes in specific microbial communities (Coriobacteriaceae, B. adolescentis, Lachnobacterium) have been related with an increase the secretion of GLP-1 and its beneficial effects.

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