Abstract
ABSTRACTObjective: The link between metabolic derangement of the gut–2013liver–visceral white adipose tissue (v-WAT) axis and gut microbiota was investigated.Methods: Rats were fed a fructose-rich diet and treated with an antibiotic mix. Inflammation was measured in portal plasma, ileum, liver, and v-WAT, while insulin signalling was analysed by measuring levels of phosphorylated kinase Akt. The function and oxidative status of hepatic mitochondria and caecal microbiota composition were also evaluated.Results: Ileal inflammation, increase in plasma transaminases, plasma peroxidised lipids, portal concentrations of tumour necrosis factor alpha, lipopolysaccharide, and non-esterified fatty acids, were induced by fructose and were reversed by antibiotic. The increased hepatic ceramide content, inflammation and decreased insulin signaling in liver and v-WAT induced by fructose was reversed by antibiotic. Antibiotic also blunted the increase in hepatic mitochondrial efficiency and oxidative damage of rats fed fructose-rich diet. Three genera, Coprococcus, Ruminococcus, and Clostridium, significantly increased, while the Clostridiaceae family significantly decreased in rats fed a fructose-rich diet, and antibiotic abolished these variationsConclusions: When gut microbiota modulation by fructose is prevented by antibiotic, inflammatory flow from the gut to the liver and v-WAT are reversed.
Highlights
Nutrient intake is a fundamental determinant of health
Energy intake and faecal energy loss were similar in the four groups of rats, while energy and lipid gain were significantly higher in fructose-fed rats than in controls, with no effect of antibiotic treatment (Table 2)
The results of the glucose tolerance test indicate that the insulin response during the first 30 min was significantly higher in fructose-fed rats than in controls (Figure 1(C))
Summary
Nutrient intake is a fundamental determinant of health. Many studies have correlated excess fructose intake with detrimental health outcomes, such as the metabolic syndrome [1,2]. Using adult rats as an animal model, we have previously shown that obesity and insulin resistance are elicited by a fructose-rich diet [3,4,5,6,7]. A body of literature has reported that some components of the diet could exert a profound influence on the composition of gut microbiota, which has been shown to play a primary role in maintaining health. Changes in the composition of the gut microbiota induced by a high-fat diet are involved in the onset of obesity and the accompanying lowgrade inflammation [8]. Less is known about the putative link between the gut microbiota and fructose-rich diets. It has been proposed that continuous exposure to fructose may cause dysbiosis, with loss of microbial genetic and phylogenic diversity, promoting the evolution and maintenance of a ‘Western’ gut microbiome [9]
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