Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent

Hamilton, M. Kristina; Boudry, Gaëlle; Lemay, Danielle G.; Raybould, Helen E.

doi:10.1152/ajpgi.00029.2015

Cited by 263 publications

(237 citation statements)

References 54 publications

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“…Here, we found that HF diet alters the composition of the fecal and cecal microbiota even after a short-term (30 d) consumption, as previously shown (38,39,43). Moreover, when we specifically analyzed the microbiota associated to the ileal mucosa, we found that HF diet favored emergence of the genus Akkermensia, a finding supported by similar observations in rat models (43,71). Akkermansia members, and more specifically Akkermansia muciniphila, have been identified as mucin-degrading bacteria residing in the mucus layer (72).…”

Section: Discussionsupporting

confidence: 86%

“…Studies have shown that, on the basis of long-term administration (9-22 wk), obesogenic diets, such as HF diet, reduce the diversity and richness of the fecal and cecal microbiota (32,68), altering the Firmicutes/Bacteroidetes balance by increasing Firmicutes (Erysipelotrichaceae), Verrucomicrobia, and decreasing Bacteroidales S24-7 (69,70). Here, we found that HF diet alters the composition of the fecal and cecal microbiota even after a short-term (30 d) consumption, as previously shown (38,39,43). Moreover, when we specifically analyzed the microbiota associated to the ileal mucosa, we found that HF diet favored emergence of the genus Akkermensia, a finding supported by similar observations in rat models (43,71).…”

Section: Discussionsupporting

confidence: 85%

“…Interestingly, most studies have characterized the fecal or cecal luminal microbiota; however, very few have attempted to characterize the mucosa-associated microbiota in the upper digestive segments, even though basic functions performed by the SI need to be tightly preserved to maintain health. As a consequence, the direct impact of HF diet initiation on SI mucosal defenses, or on the spatial distribution of the SI microbiota, remain poorly characterized and very few studies have attempted to describe the simultaneous impacts of a HF diet on IECs and on microbiota before the development of metabolic diseases (43,44).…”

Section: Significancementioning

confidence: 99%

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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.

198

146

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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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Section: Discussionsupporting

confidence: 86%

Section: Discussionsupporting

confidence: 85%

Section: Significancementioning

confidence: 99%

See 1 more Smart Citation

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.

198

146

View full text Add to dashboard Cite

show abstract

“…The microbiota has been found to be required for almost all animal models of obesity (30), and may play a role in the vagal and hypothalamic inflammation that accompanies leptin resistance, hyperphagia and the onset of overweight in susceptible animals (31)(32)(33)(34)(35)(36). Microbial transplants have been shown able to transfer the phenotypes of both overweight and liver pathology / altered blood sugar regulation to lean germ-free mice, suggesting a potentially causal role of bacteria (37)(38)(39).…”

Section: The Gastrointestinal Microbiota and The Immune Systemmentioning

confidence: 99%

“…These effects could be reversed by the addition of the missing enzyme to food. Such animal models suggest that the ability of microbial products to traverse the gut barrier -perhaps to the immune surveillance of the gutassociated lymphoid tissue, may be a key determinant of the development of obesity and metabolic issues (36,43).…”

Section: The Gastrointestinal Microbiota and The Immune 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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Connection between gut microbiome and brain development in preterm infants

Lü

Claud

2018

Developmental Psychobiology

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Dysbiosis of the gut microbiome in preterm infants predisposes the neonate to various major morbidities including neonatal necrotizing enterocolitis and sepsis in the neonatal intensive care unit, and adverse neurological outcomes later in life. There are parallel early developmental windows for the gut microbiota and the nervous system during prenatal to postnatal of life. Therefore, preterm infants represent a unique population in which optimization of initial colonization and microbiota development can affect brain development and enhance neurological outcomes. In this review, we will first discuss the factors affecting the assembly of neonatal gut microbiota and the contribution of dysbiosis in preterm infants to neuroinflammation and neurodevelopmental disorders. We then will discuss the emerging pathways connecting the gut microbiome and brain development. Further we will discuss the significance of current models for alteration of the gut microbiome (including humanized gnotobiotic models and exposure to antibiotics) to brain development and functions. Understanding the role of early optimization of the microbiome in brain development is of paramount importance for developing microbiome‐targeted therapies and protecting infants from prematurity‐related neurodevelopmental diseases.

show abstract

Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent

Abstract: Hamilton MK, Boudry G, Lemay DG, Raybould HE. Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent.

Cited by 263 publications

References 54 publications

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

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

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

Connection between gut microbiome and brain development in preterm infants

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