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- Title
H. pylori eradication with antibiotic treatment causes changes in glucose homeostasis related to modifications in the gut microbiota.
- Authors
Martín-Núñez, Gracia Mª; Cornejo-Pareja, Isabel; Coin-Aragüez, Leticia; Roca-Rodríguez, Mª del Mar; Muñoz-Garach, Araceli; Clemente-Postigo, Mercedes; Cardona, Fernando; Moreno-Indias, Isabel; Tinahones, Francisco J.
- Abstract
Background: H. pylori infection and eradication cause perturbations of the gut microbiome. The gut microbiota has been identified as a potential contributor to metabolic diseases. We evaluate whether these alterations in intestinal microbiota composition produced by H. pylori infection and its posterior eradication with antibiotic treatment could be associated with glucose homeostasis in metabolically healthy subjects. Methods: Forty adult patients infected with H. pylori and 20 control subjects were recruited. The infected subjects were evaluated before and two months after eradication treatment (omeprazole, clarithromycin, amoxicillin). The microbiota composition in fecal samples was determined by 16S rRNA gene (V3-V4) sequencing using Illumina Miseq. Results: Patients (pre- and post-H. pylori eradication) showed a decreased bacterial richness and diversity with respect to controls. There was an improvement in glucose homeostasis in subjects two months after H. pylori eradication treatment. Changes in the amount of Rikenellaceae, Butyricimonas, E. biforme, B. fragilis, and Megamonas were inversely associated with changes in the glucose level or related parameters (Hb1ac) in H. pylori eradication subjects. Conclusions: H. pylori infection and eradication with antibiotic treatment causes alteration of the human gut microbiome. The increase in SCFA-producing bacteria and glucose-removing bacteria, specifically members of Megamonas, Rikenellaceae and Butyricimonas, has been related with an improvement in glucose homeostasis after H. pylori eradication with antibiotic treatment.
- Subjects
CLARITHROMYCIN; HELICOBACTER pylori; GLUCOSE
- Publication
PLoS ONE, 2019, Vol 14, Issue 3, p1
- ISSN
1932-6203
- Publication type
Article
- DOI
10.1371/journal.pone.0213548