High-fat diet alters gut microbiota physiology in mice

Daniel, Hannelore; Gholami, Amin Moghaddas; Berry, David; Desmarchelier, Charles; Hahne, Hannes; Loh, Gunnar; Mondot, Stanislas; Lepage, Patricia; Rothballer, Michael; Walker, Alesia; Böhm, Christoph; Wenning, Mareike; Wagner, Michael; Blaut, Michaël; Schmitt‐Kopplin, Philippe; Küster, Bernhard; Haller, Dirk; Clavel, Thomas

doi:10.1038/ismej.2013.155

Cited by 556 publications

(430 citation statements)

References 86 publications

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“…18 Diet can greatly affect the GI microbiota. 74,75 The data here demonstrate that food and water deprivation is able to affect the community structure of the mucosal associated microbiota in comparison with undisturbed controls, while also affecting the abundances of select bacterial groups in the lumen. This confirms a previous study that showed separate clustering of control mice from FWD mice after a single 16-hr period of food and water deprivation.…”

Section: Discussionmentioning

confidence: 69%

The structures of the colonic mucosa-associated and luminal microbial communities are distinct and differentially affected by a prolonged murine stressor

Galley

Yu²,

Kumar

et al. 2014

Gut Microbes

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The commensal microbiota of the human gastrointestinal tract live in a largely stable community structure, assisting in host physiological and immunological functions. Changes to this structure can be injurious to the health of the host, a concept termed dysbiosis. Psychological stress is a factor that has been implicated in causing dysbiosis, and studies performed by our lab have shown that restraint stress can indeed shift the cecal microbiota structure as well as increase the severity of a colonic infection caused by Citrobacter rodentium. However, this study, like many others, have focused on fecal contents when examining the effect of dysbiosis-causing stimuli (e.g. psychological stress) upon the microbiota. Since the mucosa-associated microbiota have unique properties and functions that can act upon the host, it is important to understand how stressor exposure might affect this niche of bacteria. To begin to understand whether chronic restraint stress changes the mucosa-associated and/or luminal microbiota mice underwent 7 16-hour cycles of restraint stress, and the microbiota of both colonic tissue and fecal contents were analyzed by sequencing using nextgen bacterial tag-encoded FLX amplicon technology (bTEFAP) pyrosequencing. Both control and stress groups had significantly different mucosa-associated and luminal microbiota communities, highlighting the importance of focusing gastrointestinal community structure analysis by microbial niche. Furthermore, restraint stress was able to disrupt both the mucosa-associated and luminally-associated colonic microbiota by shifting the relative abundances of multiple groups of bacteria. Among these changes, there was a significant reduction in the immunomodulatory commensal genus Lactobacillus associated with colonic mucosa. The relative abundance of Lactobacillus spp. was not affected in the lumen. These results indicate that stressor-exposure can have distinct effects upon the colonic microbiota situated at the mucosal epithelium in comparison to the luminal-associated microbiota.

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Section: Discussionmentioning

confidence: 69%

The structures of the colonic mucosa-associated and luminal microbial communities are distinct and differentially affected by a prolonged murine stressor

Galley

Yu²,

Kumar

et al. 2014

Gut Microbes

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“…Many of these studies investigated the particular role of metabolites in inflammatory bowel diseases by using primarily NMR studies (Lin et al, 2011). Non-targeted metabolomics approaches in gut microbial sample matrices and liver, analysing changes occurring in metabolic diseases like obesity, are rarely given, but many studies addressed obesity-related metabolome characterization (Dumas et al, 2006;Williams et al, 2006;Fearnside et al, 2008;Li et al, 2008Li et al, , 2010aShearer et al, 2008;Newgard et al, 2009;Waldram et al, 2009;Kim et al, 2009Kim et al, , 2010Kim et al, , 2011Calvani et al, 2010;Xie et al, 2010Xie et al, , 2012Zhao et al, 2010;Oberbach et al, 2011;Duggan et al, 2011a,b;Jung et al, 2012;Hanhineva et al, 2013;Schäfer et al, 2014;Seyfried et al, 2013;Won et al, 2013;Xu et al, 2013;Daniel et al, 2014;Eisinger et al, 2014). Comparing with other studies, our study provides a greater insight into different metabolite classes that were involved in obesity-related changes by reflecting both bacterial and host metabolism.…”

Section: Discussionmentioning

confidence: 99%

Distinct signatures of host–microbial meta-metabolome and gut microbiome in two C57BL/6 strains under high-fat diet

et al. 2014

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A combinatory approach using metabolomics and gut microbiome analysis techniques was performed to unravel the nature and specificity of metabolic profiles related to gut ecology in obesity. This study focused on gut and liver metabolomics of two different mouse strains, the C57BL/6J (C57J) and the C57BL/6N (C57N) fed with high-fat diet (HFD) for 3 weeks, causing dietinduced obesity in C57N, but not in C57J mice. Furthermore, a 16S-ribosomal RNA comparative sequence analysis using 454 pyrosequencing detected significant differences between the microbiome of the two strains on phylum level for Firmicutes, Deferribacteres and Proteobacteria that propose an essential role of the microbiome in obesity susceptibility. Gut microbial and liver metabolomics were followed by a combinatory approach using Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS) and ultra performance liquid chromatography time of tlight MS/MS with subsequent multivariate statistical analysis, revealing distinctive host and microbial metabolome patterns between the C57J and the C57N strain. Many taurine-conjugated bile acids (TBAs) were significantly elevated in the cecum and decreased in liver samples from the C57J phenotype likely displaying different energy utilization behavior by the bacterial community and the host. Furthermore, several metabolite groups could specifically be associated with the C57N phenotype involving fatty acids, eicosanoids and urobilinoids. The mass differences based metabolite network approach enabled to extend the range of known metabolites to important bile acids (BAs) and novel taurine conjugates specific for both strains. In summary, our study showed clear alterations of the metabolome in the gastrointestinal tract and liver within a HFD-induced obesity mouse model in relation to the host-microbial nutritional adaptation.

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“…Indeed, dietary fat accounts for food imbalance, leading to obesity, and various mouse models point to gut dysbiosis as a contributing factor to obesity (30)(31)(32) and type 2 diabetes (33,34). More recently, metagenomic analysis has shown that a dysbiotic human fecal microbiota was associated with obesity, diabetes, and metabolic syndrome (35).…”

Section: Significancementioning

confidence: 99%

High-fat diet modifies the PPAR-γ pathway leading to disruption of microbial and physiological ecosystem in murine small intestine

Tomas

Mulet

Saffarian

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

193

137

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Diet is among the most important factors contributing to intestinal homeostasis, and basic functions performed by the small intestine need to be tightly preserved to maintain health. Little is known about the direct impact of high-fat (HF) diet on small-intestinal mucosal defenses and spatial distribution of the microbiota during the early phase of its administration. We observed that only 30 d after HF diet initiation, the intervillous zone of the ileum—which is usually described as free of bacteria—became occupied by a dense microbiota. In addition to affecting its spatial distribution, HF diet also drastically affected microbiota composition with a profile characterized by the expansion of Firmicutes (appearance of Erysipelotrichi), Proteobacteria (Desulfovibrionales) and Verrucomicrobia, and decrease of Bacteroidetes (family S24-7) and Candidatus arthromitus. A decrease in antimicrobial peptide expression was predominantly observed in the ileum where bacterial density appeared highest. In addition, HF diet increased intestinal permeability and decreased cystic fibrosis transmembrane conductance regulator (Cftr) and the Na-K-2Cl cotransporter 1 (Nkcc1) gene and protein expressions, leading to a decrease in ileal secretion of chloride, likely responsible for massive alteration in mucus phenotype. This complex phenotype triggered by HF diet at the interface between the microbiota and the mucosal surface was reversed when the diet was switched back to standard composition or when mice were treated for 1 wk with rosiglitazone, a specific agonist of peroxisome proliferator-activated receptor-γ (PPAR-γ). Moreover, weaker expression of antimicrobial peptide-encoding genes and intervillous bacterial colonization were observed in Ppar-γ–deficient mice, highlighting the major role of lipids in modulation of mucosal immune defenses.

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High-fat diet alters gut microbiota physiology in mice

Cited by 556 publications

References 86 publications

The structures of the colonic mucosa-associated and luminal microbial communities are distinct and differentially affected by a prolonged murine stressor

The structures of the colonic mucosa-associated and luminal microbial communities are distinct and differentially affected by a prolonged murine stressor

Distinct signatures of host–microbial meta-metabolome and gut microbiome in two C57BL/6 strains under high-fat diet

High-fat diet modifies the PPAR-γ pathway leading to disruption of microbial and physiological ecosystem in murine small intestine

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