Abstract

BackgroundAlterations in the composition of gut microbiota - known as dysbiosis - has been proposed to contribute to the development of obesity, thereby supporting the potential interest of nutrients targeting the gut with beneficial effect for host adiposity. We test the ability of a specific concentrate of water-extractable high molecular weight arabinoxylans (AX) from wheat to modulate both the gut microbiota and lipid metabolism in high-fat (HF) diet-induced obese mice.Methodology/Principal FindingsMice were fed either a control diet (CT) or a HF diet, or a HF diet supplemented with AX (10% w/w) during 4 weeks. AX supplementation restored the number of bacteria that were decreased upon HF feeding, i.e. Bacteroides-Prevotella spp. and Roseburia spp. Importantly, AX treatment markedly increased caecal bifidobacteria content, in particular Bifidobacterium animalis lactis. This effect was accompanied by improvement of gut barrier function and by a lower circulating inflammatory marker. Interestingly, rumenic acid (C18:2 c9,t11) was increased in white adipose tissue due to AX treatment, suggesting the influence of gut bacterial metabolism on host tissue. In parallel, AX treatment decreased adipocyte size and HF diet-induced expression of genes mediating differentiation, fatty acid uptake, fatty acid oxidation and inflammation, and decreased a key lipogenic enzyme activity in the subcutaneous adipose tissue. Furthermore, AX treatment significantly decreased HF-induced adiposity, body weight gain, serum and hepatic cholesterol accumulation and insulin resistance. Correlation analysis reveals that Roseburia spp. and Bacteroides/Prevotella levels inversely correlate with these host metabolic parameters.Conclusions/SignificanceSupplementation of a concentrate of water-extractable high molecular weight AX in the diet counteracted HF-induced gut dysbiosis together with an improvement of obesity and lipid-lowering effects. We postulate that hypocholesterolemic, anti-inflammatory and anti-obesity effects are related to changes in gut microbiota. These data support a role for wheat AX as interesting nutrients with prebiotic properties related to obesity prevention.

Highlights

  • Recent studies demonstrated that diet-induced obesity was linked to changes in the gut microbial ecology, resulting in an increased capacity of the distal gut microbiota to promote host adiposity [1,2]

  • We have previously shown that inulin-type fructans, non-digestible carbohydrates obtained from chicory root, restore the drop of bifidobacteria numbers occurring in the caecocolon of high fat/carbohydrate-free diet-fed mice and thereby improves metabolic alterations associated with obesity, including dyslipidemia, impaired gut permeability, endotoxemia, inflammation and diabetes [3,4,5,6]

  • We show that feeding mice with a HF diet decreases the dominant members of the mouse intestinal microbiota - Bacteroides-Prevotella ssp. from the Bacteroidetes phylum together with the specific populations of clostridial cluster XIVa, i.e. Roseburia spp from the Firmicutes phylum

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Summary

Introduction

Recent studies demonstrated that diet-induced obesity was linked to changes in the gut microbial ecology, resulting in an increased capacity of the distal gut microbiota to promote host adiposity [1,2]. Other non-digestible/fermented carbohydrates, which are gradually fermented throughout the colon and which can be applied in different food matrices, may be valuable alternative substrates to test for their health effects related to their influence on gut microbiota composition. The purpose of this study was to examine the effects of an AX concentrate, containing long-chain waterextractable AX, on the gut microbiota and lipid metabolism with focus on the expression of genes relevant to energy homeostasis and fat storage in a mice model of HF diet-induced obesity. We test the ability of a specific concentrate of water-extractable high molecular weight arabinoxylans (AX) from wheat to modulate both the gut microbiota and lipid metabolism in high-fat (HF) diet-induced obese mice

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