Rescue of Fructose-Induced Metabolic Syndrome by Antibiotics or Faecal Transplantation in a Rat Model of Obesity

PLoS One. 2015 Aug 5;10(8):e0134893. doi: 10.1371/journal.pone.0134893. eCollection 2015.

Abstract

A fructose-rich diet can induce metabolic syndrome, a combination of health disorders that increases the risk of diabetes and cardiovascular diseases. Diet is also known to alter the microbial composition of the gut, although it is not clear whether such alteration contributes to the development of metabolic syndrome. The aim of this work was to assess the possible link between the gut microbiota and the development of diet-induced metabolic syndrome in a rat model of obesity. Rats were fed either a standard or high-fructose diet. Groups of fructose-fed rats were treated with either antibiotics or faecal samples from control rats by oral gavage. Body composition, plasma metabolic parameters and markers of tissue oxidative stress were measured in all groups. A 16S DNA-sequencing approach was used to evaluate the bacterial composition of the gut of animals under different diets. The fructose-rich diet induced markers of metabolic syndrome, inflammation and oxidative stress, that were all significantly reduced when the animals were treated with antibiotic or faecal samples. The number of members of two bacterial genera, Coprococcus and Ruminococcus, was increased by the fructose-rich diet and reduced by both antibiotic and faecal treatments, pointing to a correlation between their abundance and the development of the metabolic syndrome. Our data indicate that in rats fed a fructose-rich diet the development of metabolic syndrome is directly correlated with variations of the gut content of specific bacterial taxa.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Bacterial Agents / pharmacology*
  • Bacteria / classification
  • Bacteria / genetics
  • Blood Glucose / metabolism
  • Blotting, Western
  • Cecum / drug effects
  • Cecum / metabolism
  • Cecum / microbiology
  • Diet
  • Disease Models, Animal
  • Fatty Acids, Nonesterified / blood
  • Fecal Microbiota Transplantation / methods*
  • Fructose / administration & dosage
  • Fructose / adverse effects*
  • Fructose / metabolism
  • Glucose / metabolism
  • Lipid Peroxides / metabolism
  • Liver / metabolism
  • Male
  • Metabolic Syndrome / etiology
  • Metabolic Syndrome / metabolism
  • Metabolic Syndrome / therapy*
  • Microbiota / drug effects
  • Microbiota / genetics
  • Muscle, Skeletal / metabolism
  • Obesity / etiology
  • Obesity / metabolism
  • Obesity / therapy*
  • Protein Carbonylation
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Ribosomal, 16S / genetics
  • Rats, Sprague-Dawley

Substances

  • Anti-Bacterial Agents
  • Blood Glucose
  • Fatty Acids, Nonesterified
  • Lipid Peroxides
  • RNA, Ribosomal, 16S
  • Fructose
  • Proto-Oncogene Proteins c-akt
  • Glucose

Grant support

This work was supported by the Universita Federico II di napoli, Project FARO. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.