Abstract

High fructose consumption is one of the hallmarks of Western diets and has been found to induce MeS symptoms in parallel to gut microbial dysbiosis. However, the causality between those two is still elusive. Here, we studied whether a significant modification of gut microbial composition by antibiotics can influence the fructose-induced metabolic changes. Male Sprague-Dawley (SD) rats were divided into four groups including controls, controls + antibiotics, high fructose diet (HFrD, 60% fructose), HFrD + antibiotics (n = 7–8 in each group) for a period of 8-weeks. The high fructose diet increased blood pressure (BP), triglyceride (TG), fatty liver and the expression of hepatic genes related to lipogenesis, and fructose transport and metabolism. In addition, fructose changed the microbial composition and increased acetic and butyric acids in fecal samples but not in the blood. Antibiotic treatment significantly reduced microbial diversity and modified the microbial composition in the samples. However, minimal or no effect was seen in the metabolic phenotypes. In conclusion, high fructose consumption (60%) induced metabolic changes and dysbiosis in rats. However, antibiotic treatment did not reverse the metabolic phenotype. Therefore, the metabolic changes are probably independent of a specific microbiome profile.

Highlights

  • Fructose consumption has significantly increased in Western diets over the last few decades, as many prepared beverages and foods have added sucrose or high fructose corn syrup [1]

  • One mechanism by which the microbiota humanisobutyrate, health and disease is their In capacity to samples, we noted significant increase the concentration of acetic and butyricthe acids in high fructose diet (HFrD), produce by afermenting dietary in fibers

  • In the fecal isobutyric acids concentrations were significantly lower in rats treated with antibiotics compared samples, we noted a significant increase in the concentration of acetic and butyric acids in HFrD, to HFrD

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Summary

Introduction

Fructose consumption has significantly increased in Western diets over the last few decades, as many prepared beverages and foods have added sucrose or high fructose corn syrup [1]. Western diet consumption is linked to metabolic syndrome (MeS) and diabetes mellitus type 2 (T2DM). High fructose diets rapidly cause features of MeS including: dyslipidemia, fatty liver, hypertension, insulin resistance and glucose intolerance. Short term fructose feeding in humans increases triglyceride levels and insulin resistance that are not observed with equivalent amounts of glucose [5,6,7]. The conclusion of these studies is that fructose ingestion can significantly contribute to metabolic syndrome development [8].

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