298-LB: GLP-1 Secretion Enhancement after H. Pylori Eradication Treatment Is Related to Gut Microbiota Modification

Abstract

Introduction: Antibiotic treatments modify gut microbiota. Microbiota alterations (in composition and biodiversity) are fundamental pieces in the development of metabolic disorders (T2DM and obesity). Objective: To evaluate the relationship between microbiota changes due to antibiotic treatment in patients colonized by H. pylori and GLP-1 secretion. Methods: A prospective case control study was assessed. We evaluated a H. pylori positive patient model before and two months after a short-term eradication therapy and a control group. Anthropometric measurements, carbohydrate and lipid metabolisms, GLP-1 levels and fecal microbiota composition (determined by 16S rRNA gene (V3-V4) sequencing with an Illumina Miseq) were analyzed. Results: We studied 40 cases and 20 controls (60% women, respectively). Average age was 47.0±2 vs. 43.6±2.7 years. 42.5% vs. 40% had clinical history of gastrointestinal disease. After eradication treatment, we found significant changes in microbiota profile at phylum, family, genus and species levels. The Chao1 and Shannon indices showed a decreased in bacterial richness and diversity in patients (pre and post H. pylori eradication) compared to controls. GLP-1 secretion and carbohydrate metabolism were improved after antibiotic treatment. GLP-1 changes were related to microbial community disturbances through correlation analysis, specifically with Bifidobacterium adolescentis (r=0.354, p=0.034), Lachnobacterium (r=-0.332, p=0.048) and Coriobacteriaceae (r=0.372, p=0.026). Conclusions: Antibiotic treatment to eradicate H. pylori increased the secretion of GLP-1 and improved the carbohydrate metabolism. This GLP-1 secretion improvement was related to changes in microbial community because of the antibiotic treatment, particularly in Bifidobacterium adolescentis, Lachnobacterium and Coriobacteriaceae. These taxa could play their roles through the production of short chain fatty acids (SCFA) and/or bile acid metabolism. Disclosure I. Cornejo-Pareja: None. G. Martin-Nuñez: None. I. Moreno-Indias: None. F.F. Cardona-Díaz: None. M. Roca-Rodriguez: None. L. Coin-Arangüez: None. I. Mancha-Doblas: None. F. Tinahones: Advisory Panel; Self; Lilly Diabetes, Novo Nordisk A/S, Regeneron Pharmaceuticals, Sanofi-Aventis. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. Speaker’s Bureau; Self; Danone Nutricia Research, Lilly Diabetes, Novo Nordisk A/S, Regenerative Medical Solutions, Sanofi-Aventis.