Limits...
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 do not affect the fructose-induced increase in body energy and lipid content.Animal whole body composition was obtained by measurement of body energy (panel A), lipids (panel B) and epididymal fat (C) content in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats. Values are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4526532&req=5

pone.0134893.g001: Antibiotics or faecal samples do not affect the fructose-induced increase in body energy and lipid content.Animal whole body composition was obtained by measurement of body energy (panel A), lipids (panel B) and epididymal fat (C) content in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats. Values are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test).

Mentions: A first metabolic characterization was carried out by analyzing the animal whole body composition. As shown in Fig 1, fructose-fed rats displayed significantly higher body energy (panel A), lipids (panel B) and epididymal fat compared to controls. The treatment with antibiotics or faecal samples did not affect the increase in body energy (Fig 1A) or lipids (Fig 1B and 1C) due to the diet. No significant difference was found in final body weight (C = 538±20; CA = 540±15; F = 541±15; FA = 537±17; FT = 540±23 g) and in body weight gain (C = 78±5; CA = 80±5; F = 81±8; FA = 77±7; FT = 80±3 g) between the five groups of rats. Since changes in energy intake are the primary drive of obesity development, metabolisable energy (ME) intake was monitored throughout the experimental period to verify whether the fructose-induced increase in body energy and lipid content was due to an increase of ME. To this aim, food intake and energy loss through faeces and urines were analyzed (Methods) and indicated that ME intake was similar in all experimental groups (C = 19,700±1,200 kJ, CA = 19,400±1,050 kJ, F = 19,500±1,100 kJ, FA = 19,200±990 kJ, FT = 19,500±1,000 kJ). In addition, the caecal content of glucose and fructose was measured to assess whether dietary treatment could modify substrate availability in the hindgut, but no significant variation en caecal glusose and fructose was found between the five groups of rats (S1 Table).


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 do not affect the fructose-induced increase in body energy and lipid content.Animal whole body composition was obtained by measurement of body energy (panel A), lipids (panel B) and epididymal fat (C) content in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats. Values are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0134893.g001: Antibiotics or faecal samples do not affect the fructose-induced increase in body energy and lipid content.Animal whole body composition was obtained by measurement of body energy (panel A), lipids (panel B) and epididymal fat (C) content in control (C), control+antibiotic (CA), fructose-fed (F), fructose-fed+antibiotic (FA) and fructose-fed+faecal samples (FT) rats. Values are reported as means±SEM of six different rats. * P< .05 (one-way ANOVA followed by Tukey post-test).
Mentions: A first metabolic characterization was carried out by analyzing the animal whole body composition. As shown in Fig 1, fructose-fed rats displayed significantly higher body energy (panel A), lipids (panel B) and epididymal fat compared to controls. The treatment with antibiotics or faecal samples did not affect the increase in body energy (Fig 1A) or lipids (Fig 1B and 1C) due to the diet. No significant difference was found in final body weight (C = 538±20; CA = 540±15; F = 541±15; FA = 537±17; FT = 540±23 g) and in body weight gain (C = 78±5; CA = 80±5; F = 81±8; FA = 77±7; FT = 80±3 g) between the five groups of rats. Since changes in energy intake are the primary drive of obesity development, metabolisable energy (ME) intake was monitored throughout the experimental period to verify whether the fructose-induced increase in body energy and lipid content was due to an increase of ME. To this aim, food intake and energy loss through faeces and urines were analyzed (Methods) and indicated that ME intake was similar in all experimental groups (C = 19,700±1,200 kJ, CA = 19,400±1,050 kJ, F = 19,500±1,100 kJ, FA = 19,200±990 kJ, FT = 19,500±1,000 kJ). In addition, the caecal content of glucose and fructose was measured to assess whether dietary treatment could modify substrate availability in the hindgut, but no significant variation en caecal glusose and fructose was found between the five groups of rats (S1 Table).

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