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.
Highlights
It is well-established that a hypercaloric diet, rich in highly refined carbohydrates and fat (Western diet), can induce a wide range of metabolic alterations, including obesity, increased plasma triglyceride concentration, impaired glucose tolerance and insulin resistance [1,2,3]
To assess the contribution of skeletal muscle to changes in glucose tolerance, we investigated a distal effector of insulin signalling in this tissue, and we found that pAkt levels were significantly lower in fructose-fed and fructose-fed+faecal samples rats, while this decrease was abolished by antibiotic treatment (Fig 2D and S1 Fig)
The main result of this study is that in fructose-fed rats the development of metabolic syndrome directly correlates with the alteration of the microbial composition of the gut
Summary
It is well-established that a hypercaloric diet, rich in highly refined carbohydrates and fat (Western diet), can induce a wide range of metabolic alterations, including obesity, increased plasma triglyceride concentration, impaired glucose tolerance and insulin resistance [1,2,3]. It has been estimated that in the US the load of free fructose has increased from 158.5 kcal per person per day in 1978 to 228 kcal per person per day in 1998 [3] This substantial increase has paralleled the increased incidence of obesity, leading to the hypothesis that a fructose-rich diet may contribute to the development of obesity and related metabolic disorders [3,4,5]. The contribution of high-fructose diets to the development of obesity remains controversial, since some authors have not observed unequivocal evidence linking fructose consumption with metabolic disorders [2] To address this issue, studies with animal models have proven informative [6]. We found that long term consumption of the fructose-rich diet impaired glucose tolerance, induced an oxidative stress status and increased plasma non-esterified-fatty-acids (NEFA) [9], the latter being considered a reliable marker of the development of insulin resistance [10]
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