Dietary Supplementation with the Probiotic SF68 Reinforces Intestinal Epithelial Barrier in Obese Mice by Improving Butyrate Bioavailability

Author:

Benvenuti Laura1ORCID,D'Antongiovanni Vanessa1,Pellegrini Carolina1,Fornai Matteo1,Bernardini Nunzia12,Ippolito Chiara1,Segnani Cristina1,Di Salvo Clelia1,Colucci Rocchina3,Martelli Alma4,Flori Lorenzo4,Calderone Vincenzo4,Carta Gianfranca5,Ghelardi Emilia6,Calvigioni Marco6,Panattoni Adelaide6,Coppolecchia Raffaella7,Arini Achille7,Antonioli Luca1

Affiliation:

1. Department of Clinical and Experimental Medicine University of Pisa Pisa Italy

2. Interdepartmental Research Center “Nutraceuticals and Food for Health” University of Pisa Pisa Italy

3. Department of Pharmaceutical and Pharmacological Sciences University of Padova Padova Italy

4. Department of Pharmacy University of Pisa Pisa Italy

5. Department of Biomedical Sciences University of Cagliari Cagliari Italy

6. Department of Translational Research and New Technologies in Medicine and Surgery University of Pisa Pisa Italy

7. Cerbios Pharma‐SA Lugano Switzerland

Abstract

ScopeModifications in intestinal microbiota and its metabolites, the short‐chain fatty acids (SCFA) are main factors altering intestinal epithelial barrier integrity and eliciting the onset of a meta‐inflammation observed in obesity. The present study is aimed at evaluating the efficacy of Enterococcus faecium (SF68) administration in counteracting the impairment of gut barrier and enteric inflammation in a model of diet‐induced obesity, characterizing the molecular mechanisms underlying such beneficial effects.Methods and ResultsMale C57BL/6J mice, fed with standard diet (SD) or high‐fat diet (HFD), are treated with SF68 (108 CFU day−1). After 8 weeks, plasma interleukin (IL)‐1β and lipopolysaccharide binding protein (LBP) are measured, analysis of fecal microbiota composition and butyrate content as well as intestinal malondialdehyde, myeloperoxidase, mucins, tight junction protein, and butyrate transporter expression are investigated. After 8 weeks, SF68 administration counteracts the body weight gain in HFD mice, reducing plasma IL‐1β and LBP. In parallel, SF68 treatment acts against the intestinal inflammation in HFD‐fed animals and improves the intestinal barrier integrity and functionality in obese mice via the increase in tight junction protein and intestinal butyrate transporter (sodium‐coupled monocarboxylate transporter 1 ) expression.ConclusionsSupplementation with SF68 reduces intestinal inflammation and reinforces the enteric epithelial barrier in obese mice, improving the transport and utilization of butyrate.

Publisher

Wiley

Subject

Food Science,Biotechnology

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