Diet‐induced obesity causes metabolic impairment independent of alterations in gut barrier integrity

Kless, Caroline; Müller, Veronika Maria; Schüppel, Valentina; Lichtenegger, Martina; Rychlik, Michael; Daniel, Hannelore; Klingenspor, Martin; Haller, Dirk

doi:10.1002/mnfr.201400840

Cited by 31 publications

(23 citation statements)

References 42 publications

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“…In 2007, we found that changes in gut microbiota composition observed following HFD feeding were associated with increased plasma lipopolysaccharide (LPS) levels (the so‐called metabolic endotoxemia) , a phenomenon also extensively confirmed in other studies and in humans (Fig. ) , except in a recent study . The reason of this discrepancy is likely due to the difficulty to asses these critical parameters in complex matrix such as blood (e.g., false negative and LPS recoveries).…”

Section: Introductionmentioning

confidence: 69%

Talking microbes: When gut bacteria interact with diet and host organs

Cani

Everard

2015

Molecular Nutrition Food Res

132

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Obesity and diabetes have reached epidemic proportions. Evidence suggests that besides dietary habits and physical activity, other environmental factors, such as gut microbes, are recognized as additional partners implicated in the control of energy homeostasis. Studies on the human gut microbiota have shown that the general population can be stratified on the sole basis of three dominant bacteria (i.e., the concept of enterotypes), while some others have suggested categorizing the population according to their microbiome gene richness. Both aspects have been strengthened by recent studies investigating the impact of nutrients (e.g., dietary fibers, fat feeding) and dietary habits (i.e., vegans versus omnivores) of different populations. Using preclinical models, quite a few novel mechanisms have been proposed in these gut microbiota–host interactions, including the role of novel bacteria, the regulation of antimicrobial peptide production, the maintenance of the gut barrier function and intestinal innate immunity. In this review, we discuss several of the aforementioned aspects. Nonetheless, determining the overall mechanisms by which microbes dialogue with host cells will require further investigations before anticipating the development of next‐generation nutritional interventions using prebiotics, probiotics, synbiotics, or even specific nutrients for promoting health benefits.

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Section: Introductionmentioning

confidence: 69%

Talking microbes: When gut bacteria interact with diet and host organs

Cani

Everard

2015

Molecular Nutrition Food Res

132

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“…Mono‐association of germfree mice with the gram negative Enterobacter cloacae , which was isolated from an obese human individual, induced obesity and elevated the systemic endotoxin concentration and inflammatory markers . However, diet‐induced obesity is not necessarily associated with impaired gut barrier integrity as recently demonstrated in three inbred mouse strains . C57BL/6J mice were fed the same lard‐based HFD used by Cani et al.…”

Section: Discussionmentioning

confidence: 96%

“…, but did not reveal any gut‐barrier dysfunction. Hence, it may be speculated that the observed differences between the two studies are due to differences in microbiota composition between the animal facilities of the two laboratories . Interestingly, in humans, obesity, and the obesity‐associated microbiota are not associated with an increased gut permeability suggesting a minor contribution of gut permeability to metabolic disease and endotoxemia.…”

Section: Discussionmentioning

confidence: 99%

Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum

Woting

Pfeiffer

Hanske

et al. 2015

Molecular Nutrition Food Res

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ScopeDiet‐induced obesity is associated with changes in the gut microbiota and low‐grade inflammation. Oligofructose was reported to ameliorate high fat diet‐induced metabolic disorders in mice by restoring the number of intestinal bifidobacteria. However, this has not been experimentally demonstrated.Methods and resultsWe fed conventional mice, germfree mice, mice associated with a simplified human gut microbiota composed of eight bacterial species including Bifidobacterium longum (SIHUMI), and mice associated with SIHUMI without B. longum a low fat diet (LFD), a high fat diet (HFD), or a HFD containing 10% oligofructose (HFD + OFS) for five weeks. We assessed body composition, bacterial cell numbers and metabolites, markers of inflammation, and gut permeability. Conventional mice fed HFD or HFD + OFS did not differ in body weight gain and glucose tolerance. The gnotobiotic mouse groups fed LFD or HFD + OFS gained less body weight and body fat, and displayed an improved glucose tolerance compared with mice fed HFD. These differences were not affected by the presence of B. longum. Mice fed HFD showed no signs of inflammation or increased intestinal permeability.ConclusionThe ability of oligofructose to reduce obesity and to improve glucose tolerance in gnotobiotic mice fed HFD was independent of the presence of B. longum.

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“…Low-grade inflammation has frequently been discussed in obesity [56], [57], [58]. This observation together with the increased metabolites related to the arachidonic acid pathway in LHFD-fed GF mice led us to investigate plasma S-amyloid A levels.…”

Section: Discussionmentioning

confidence: 99%

Dietary fat and gut microbiota interactions determine diet-induced obesity in mice

Kübeck

Bonet-Ripoll

Hoffmann

et al. 2016

Molecular Metabolism

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181

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ObjectiveGut microbiota may promote positive energy balance; however, germfree mice can be either resistant or susceptible to diet-induced obesity (DIO) depending on the type of dietary intervention. We here sought to identify the dietary constituents that determine the susceptibility to body fat accretion in germfree (GF) mice.MethodsGF and specific pathogen free (SPF) male C57BL/6N mice were fed high-fat diets either based on lard or palm oil for 4 wks. Mice were metabolically characterized at the end of the feeding trial. FT-ICR-MS and UPLC-TOF-MS were used for cecal as well as hepatic metabolite profiling and cecal bile acids quantification, respectively. Hepatic gene expression was examined by qRT-PCR and cecal gut microbiota of SPF mice was analyzed by high-throughput 16S rRNA gene sequencing.ResultsGF mice, but not SPF mice, were completely DIO resistant when fed a cholesterol-rich lard-based high-fat diet, whereas on a cholesterol-free palm oil-based high-fat diet, DIO was independent of gut microbiota. In GF lard-fed mice, DIO resistance was conveyed by increased energy expenditure, preferential carbohydrate oxidation, and increased fecal fat and energy excretion. Cecal metabolite profiling revealed a shift in bile acid and steroid metabolites in these lean mice, with a significant rise in 17β-estradiol, which is known to stimulate energy expenditure and interfere with bile acid metabolism. Decreased cecal bile acid levels were associated with decreased hepatic expression of genes involved in bile acid synthesis. These metabolic adaptations were largely attenuated in GF mice fed the palm-oil based high-fat diet. We propose that an interaction of gut microbiota and cholesterol metabolism is essential for fat accretion in normal SPF mice fed cholesterol-rich lard as the main dietary fat source. This is supported by a positive correlation between bile acid levels and specific bacteria of the order Clostridiales (phylum Firmicutes) as a characteristic feature of normal SPF mice fed lard.ConclusionsIn conclusion, our study identified dietary cholesterol as a candidate ingredient affecting the crosstalk between gut microbiota and host metabolism.

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Diet‐induced obesity causes metabolic impairment independent of alterations in gut barrier integrity

Abstract: None of our results provided any evidence that gut barrier function is a subject to dietary regulation and obesity per se seems not to cause gut barrier impairment.

Cited by 31 publications

References 42 publications

Talking microbes: When gut bacteria interact with diet and host organs

Talking microbes: When gut bacteria interact with diet and host organs

Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum

Dietary fat and gut microbiota interactions determine diet-induced obesity in mice

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