Research Article: H. pylori eradication with antibiotic treatment causes changes in glucose homeostasis related to modifications in the gut microbiota

Date Published: March 14, 2019

Publisher: Public Library of Science

Author(s): Gracia Mª Martín-Núñez, Isabel Cornejo-Pareja, Leticia Coin-Aragüez, Mª del Mar Roca-Rodríguez, Araceli Muñoz-Garach, Mercedes Clemente-Postigo, Fernando Cardona, Isabel Moreno-Indias, Francisco J. Tinahones, Marie-Joelle Virolle.


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.

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.

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.

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.

Partial Text

Helicobacter pylori is a Gram-negative bacterium that colonizes the gastric mucosa of humans and non-human primates [1]. H. pylori is typically acquired early in life and the infection often persists during patients’ entire lives. The prevalence of H. pylori infection in the adult population ranges from 25–60% in Europe and up to 90% in Asia and South America, depending on geographical and infrastructural factors [2].The majority of people with H. pylori are asymptomatic and only fewer than 20% of H. pylori colonized people develop serious diseases (e.g. multifocal atrophic gastritis, gastric adenocarcinoma, mucosa-associated-lymph-tissue [MALT] lymphoma) [3–4].

In this study, we have shown that H. pylori eradication with antibiotic treatment produces specific bacterial changes associated with an improvement in glucose homeostasis and HbA1c levels in patients with normal blood glucose concentrations. HbA1c is an index of long-term glycemic control and a risk predictor used in the monitoring of diabetes. However, HbA1c levels are acquiring a big relevance also in apparently healthy subjects [25] because of its successful standardization among subjects. Our study has shown moderate changes in HbA1c between patients before and after the H. pylori eradication. However, these variations in HbA1c are statistically significant and could be clinically relevant; by analogy with other studies, these small changes are similar to those observed after life-style modifications, for example, after dietary interventions and physical exercise [26–27]. The favorable effect of H. pylori eradication on glucose homeostasis have been reported in previous studies [28–29]. However, the mechanisms underlying the association between H. pylori eradication and glucose homeostasis are unclear. We propose that gut microbiota mediated, at least partially, this improvement in the glucose homeostasis.




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