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

Di Luccia B, Crescenzo R, Mazzoli A, Cigliano L, Venditti P, Walser JC, Widmer A, Baccigalupi L, Ricca E, Iossa S - PLoS ONE (2015)

Bottom Line: Body composition, plasma metabolic parameters and markers of tissue oxidative stress were measured in all groups.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University "Federico II" of Naples, Naples, Italy.

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.

No MeSH data available.


Related in: MedlinePlus

Antibiotics or faecal samples reduce markers of the fructose-induced metabolic syndrome.Plasma NEFA (A) and inhibitory effect of insulin on lipolysis in epididymal WAT (B) were assessed as first markers of metabolic syndrome. Changes in plasma glucose after the administration of a given dose of glucose were plotted over the time (C) and the area under the curves was calculated and used to estimate glucose tolerance (inset in panel C), while the contribution of skeletal muscle to changes in glucose tolerance was estimated by measuring the degree of phosphorylation of the kinase Akt, a distal effector of insulin signalling in this tissue (D). As a third marker of the development of a metabolic syndrome, the plasma concentration of LPS (E) and TNF-alpha (F) were considered. Values obtained in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test). EU = endotoxin unit.
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pone.0134893.g002: Antibiotics or faecal samples reduce markers of the fructose-induced metabolic syndrome.Plasma NEFA (A) and inhibitory effect of insulin on lipolysis in epididymal WAT (B) were assessed as first markers of metabolic syndrome. Changes in plasma glucose after the administration of a given dose of glucose were plotted over the time (C) and the area under the curves was calculated and used to estimate glucose tolerance (inset in panel C), while the contribution of skeletal muscle to changes in glucose tolerance was estimated by measuring the degree of phosphorylation of the kinase Akt, a distal effector of insulin signalling in this tissue (D). As a third marker of the development of a metabolic syndrome, the plasma concentration of LPS (E) and TNF-alpha (F) were considered. Values obtained in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test). EU = endotoxin unit.

Mentions: The levels of plasma NEFA and glucose intolerance were followed as early markers of the development of metabolic derangement and insulin resistance. Fig 2A shows that the significant increase in plasma NEFA found in fructose-fed rats (group F vs C) was almost completely reversed by treatment with antibiotics (group FA) or faecal samples (group FT). In addition, the inhibitory effect of insulin on lipolysis in epididymal WAT was nearly absent in fructose-fed rats (group F), but was completely restored by treatment with antibiotics (group FA) or faecal samples (group FT) (Fig 2B).


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

Di Luccia B, Crescenzo R, Mazzoli A, Cigliano L, Venditti P, Walser JC, Widmer A, Baccigalupi L, Ricca E, Iossa S - PLoS ONE (2015)

Antibiotics or faecal samples reduce markers of the fructose-induced metabolic syndrome.Plasma NEFA (A) and inhibitory effect of insulin on lipolysis in epididymal WAT (B) were assessed as first markers of metabolic syndrome. Changes in plasma glucose after the administration of a given dose of glucose were plotted over the time (C) and the area under the curves was calculated and used to estimate glucose tolerance (inset in panel C), while the contribution of skeletal muscle to changes in glucose tolerance was estimated by measuring the degree of phosphorylation of the kinase Akt, a distal effector of insulin signalling in this tissue (D). As a third marker of the development of a metabolic syndrome, the plasma concentration of LPS (E) and TNF-alpha (F) were considered. Values obtained in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test). EU = endotoxin unit.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4526532&req=5

pone.0134893.g002: Antibiotics or faecal samples reduce markers of the fructose-induced metabolic syndrome.Plasma NEFA (A) and inhibitory effect of insulin on lipolysis in epididymal WAT (B) were assessed as first markers of metabolic syndrome. Changes in plasma glucose after the administration of a given dose of glucose were plotted over the time (C) and the area under the curves was calculated and used to estimate glucose tolerance (inset in panel C), while the contribution of skeletal muscle to changes in glucose tolerance was estimated by measuring the degree of phosphorylation of the kinase Akt, a distal effector of insulin signalling in this tissue (D). As a third marker of the development of a metabolic syndrome, the plasma concentration of LPS (E) and TNF-alpha (F) were considered. Values obtained in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test). EU = endotoxin unit.
Mentions: The levels of plasma NEFA and glucose intolerance were followed as early markers of the development of metabolic derangement and insulin resistance. Fig 2A shows that the significant increase in plasma NEFA found in fructose-fed rats (group F vs C) was almost completely reversed by treatment with antibiotics (group FA) or faecal samples (group FT). In addition, the inhibitory effect of insulin on lipolysis in epididymal WAT was nearly absent in fructose-fed rats (group F), but was completely restored by treatment with antibiotics (group FA) or faecal samples (group FT) (Fig 2B).

Bottom Line: Body composition, plasma metabolic parameters and markers of tissue oxidative stress were measured in all groups.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University "Federico II" of Naples, Naples, Italy.

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.

No MeSH data available.


Related in: MedlinePlus