The small intestine microbiota, nutritional modulation and relevance for health

Aidy, Sahar El; Bogert, Bartholomeus van den; Kleerebezem, Michiel

doi:10.1016/j.copbio.2014.09.005

Cited by 203 publications

(177 citation statements)

References 55 publications

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“…This suggests that differences may have existed between the upper gut microbiotas of the obese and control groups of human donors, which were not reflected in faeces. Considering that most differences in genera found in mice colon already occurred in ileum, we find it likely that the ileal microbiota plays an important role in development of the metabolic syndrome (El Aidy et al, 2015), which is in line with the fact that ileum is the main place for bile acid absorption (Dawson et al, 2009) and intestinal immunity (Jung et al, 2010). A strong positive correlation between caecal OTU richness and insulin resistance was observed (Figure 6a), whereas previous reports have linked diversity and gene richness of the faecal microbiome to a healthy metabolic status in humans (Lozupone et al, 2012;Le Chatelier et al, 2013).…”

Section: Discussionmentioning

confidence: 90%

Environmental spread of microbes impacts the development of metabolic phenotypes in mice transplanted with microbial communities from humans

et al. 2016

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Microbiota transplantation to germ-free animals is a powerful method to study involvement of gut microbes in the aetiology of metabolic syndrome. Owing to large interpersonal variability in gut microbiota, studies with broad coverage of donors are needed to elucidate the establishment of human-derived microbiotas in mice, factors affecting this process and resulting impact on metabolic health. We thus transplanted faecal microbiotas from humans (16 obese and 16 controls) separately into 64 germ-free Swiss Webster mice caged in pairs within four isolators, with two isolators assigned to each phenotype, thereby allowing us to explore the extent of microbial spread between cages in a well-controlled environment. Despite high group-wise similarity between obese and control human microbiotas, transplanted mice in the four isolators developed distinct gut bacterial composition and activity, body mass gain, and insulin resistance. Spread of microbes between cages within isolators interacted with establishment of the transplanted microbiotas in mice, and contributed to the transmission of metabolic phenotypes. Our findings highlight the impact of donor variability and reveal that inter-individual spread of microbes contributes to the development of metabolic traits. This is of major importance for design of animal studies, and indicates that environmental transfer of microbes between individuals may affect host metabolic traits.

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Section: Discussionmentioning

confidence: 90%

Environmental spread of microbes impacts the development of metabolic phenotypes in mice transplanted with microbial communities from humans

et al. 2016

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“…Various mechanisms have been described through which the intestinal microbiota may interact with mucosal immunity (Hooper et al, 2012;El Aidy et al, 2015). One key pathway is tolllike receptor (TLR) signalling, which can influence regulatory T-cell populations, the autophagy pathway (Sun et al, 2011;Frosali et al, 2015), cellular epithelial proliferation, cytoprotective effects, immune cell recruitment, IgA production and secretion of antimicrobial peptides (RakoffNahoum et al, 2004;Shang et al, 2008;El Aidy et al, 2015). It is also increasingly evident that enteric bacteria influence production of effector CD4+ T helper (Th) cells, which are imperative in protecting the gut from developing colitis (Kullberg et al, 2002;Kamada & Núñez, 2014).…”

Section: Microbiota-immune System Cross-talkmentioning

confidence: 99%

An overview of the bacterial contribution to Crohn disease pathogenesis

Alhagamhmad

Day

Lemberg

et al. 2016

Journal of Medical Microbiology

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“…An inappropriate innate immune response to these microbial changes is believed to underlie periodontitis, and may also exacerbate atherosclerosis (48,49), while limiting the sources of processed carbohydrate in diet can produce marked improvements in periodontal health (50,51). The small intestinal microbiota is proximal to both the satiety-sensing vagal afferents believed to play a key role in energy-homeostasis(52) (35), and to the immune system hub of the gut-associated lymphoid tissue (53,54). Hence, pro-inflammatory microbial ecosystem changes in the small intestine, analogous to those reported in the mouth, and likewise produced by powdered carbohydrates, would be an excellent candidate mechanism to initiate obesity, metabolic syndrome and a wide range of systemic immune dysregulatory effects (24).…”

Section: Microbes As Sensors Of Dietary Refinement -Dental and Systemmentioning

confidence: 99%

Dietary Refinement And The Upper Gut Microbiota: The Starting Point For Obesity And Non-Communicable Diseases?

Spreadbury¹

2017

jevohealth

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IntroductionThe epidemics of obesity and related non-communicable diseases remains a matter of the utmost concern for public health(1). While physical exercise has been shown able to provide concrete benefits(2,3), there is good reason to believe that it cannot fully compensate for the deleterious changes produced by poor diet(4). Opinions regarding optimal diet increasingly show elements of convergence, especially regarding the association of dietary refinement and ultra-processed foods with poorer health outcomes(5). Some proposed mechanisms underlying this epidemiology of junk food include the removal from diet of health-promoting compounds due to inadequate fruit and vegetable consumption(6), and the enhancement of glycemic responses by the refinement of foods(7-9). Consistent with the latter, ad libitum low-carbohydrate diets (<50 g / day) have been shown to produce weight loss(10,11) and improve cardiovascular risk profiles(12). However, some very high carbohydrate diets have also been shown to be compatible with population-wide optimal metabolic health in non-cereal agrarian populations(13-16). Likewise, the "paleolithic style" diets used to date in small clinical trials have achieved consensus diet-beating improvements in metabolic and cardiovascular-disease risk factors(17-21) despite not restricting total carbohydrate into the <50 g / day range. Similar short-term benefits have also been shown for "the McDougall Program" a low fat, high carbohydrate diet that places a strong emphasis on food quality and minimizes processed carbohydrates(22). This wide range of carbohydrate content for ad libitum diets that produce weight loss suggests that low glycemic index and minimized insulin release are not credible explanations for their effects, especially in light of the experimental variability in the glycemic index of foods between individuals and between meal contexts(23). However, one factor that these dietary regimens do have in common is minimal consumption of processed foods, milled flours and sugar. The present article is an outline of a recently proposed mechanism(24,25) that could explain the effects of food-quality upon weight and health, independent of overall macronutrient composition.

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The small intestine microbiota, nutritional modulation and relevance for health

Cited by 203 publications

References 55 publications

Environmental spread of microbes impacts the development of metabolic phenotypes in mice transplanted with microbial communities from humans

Environmental spread of microbes impacts the development of metabolic phenotypes in mice transplanted with microbial communities from humans

An overview of the bacterial contribution to Crohn disease pathogenesis

Dietary Refinement And The Upper Gut Microbiota: The Starting Point For Obesity And Non-Communicable Diseases?

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