scholarly journals The Woodrat Gut Microbiota as an Experimental System for Understanding Microbial Metabolism of Dietary Toxins

2016 ◽  
Vol 7 ◽  
Author(s):  
Kevin D. Kohl ◽  
M. Denise Dearing
Keyword(s):  
Gut Microbiota ◽  
Experimental System ◽  
Microbial Metabolism ◽  
Dietary Toxins

scholarly journals Honeybee gut microbiota promotes host weight gain via bacterial metabolism and hormonal signaling

2017 ◽  
Vol 114 (18) ◽  
pp. 4775-4780 ◽  
Author(s):  
Hao Zheng ◽  
J. Elijah Powell ◽  
Margaret I. Steele ◽  
Carsten Dietrich ◽  
Nancy A. Moran
Keyword(s):  
Weight Gain ◽  
Gut Microbiota ◽  
Microbial Metabolism ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Whole Body ◽  
Social Bees ◽  
Host Microbe Interactions ◽  
The Impact

Social bees harbor a simple and specialized microbiota that is spatially organized into different gut compartments. Recent results on the potential involvement of bee gut communities in pathogen protection and nutritional function have drawn attention to the impact of the microbiota on bee health. However, the contributions of gut microbiota to host physiology have yet to be investigated. Here we show that the gut microbiota promotes weight gain of both whole body and the gut in individual honey bees. This effect is likely mediated by changes in host vitellogenin, insulin signaling, and gustatory response. We found that microbial metabolism markedly reduces gut pH and redox potential through the production of short-chain fatty acids and that the bacteria adjacent to the gut wall form an oxygen gradient within the intestine. The short-chain fatty acid profile contributed by dominant gut species was confirmed in vitro. Furthermore, metabolomic analyses revealed that the gut community has striking impacts on the metabolic profiles of the gut compartments and the hemolymph, suggesting that gut bacteria degrade plant polymers from pollen and that the resulting metabolites contribute to host nutrition. Our results demonstrate how microbial metabolism affects bee growth, hormonal signaling, behavior, and gut physicochemical conditions. These findings indicate that the bee gut microbiota has basic roles similar to those found in some other animals and thus provides a model in studies of host–microbe interactions.

scholarly journals The gut microbial metabolome: modulation of cancer risk in obese individuals

2012 ◽  
Vol 72 (1) ◽  
pp. 178-188 ◽  
Author(s):  
Wendy R. Russell ◽  
Sylvia H. Duncan ◽  
Harry J. Flint
Keyword(s):  
Gut Microbiota ◽  
Genetic Factors ◽  
Microbial Metabolism ◽  
Health Concern ◽  
Human Gut ◽  
Alcoholic Fatty Liver ◽  
Health And Disease ◽  
Diet And Lifestyle ◽  
Alcoholic Fatty Liver Disease

Obesity is a critical health concern and although genetic factors may predispose an individual to become obese, changes in diet and lifestyle over the last few decades are likely to be significant contributors. Even so, it has been suggested that the causes of the current obesity crisis are not simply explained by changes in eating and exercise habits. Evidence suggests that the gut microbiota may play an important role in obesity and may be a factor in the development of associated disease including diabetes, CVD, non-alcoholic fatty liver disease and cancer. There have been tremendous advances in knowledge regarding the composition of human gut microbiota, but less is known about their function and role within the human host. It is becoming widely accepted that the products of microbial metabolism influence human health and disease, particularly with respect to immune response and inflammation. However, in most cases, the products of microbial metabolism are uncharacterised and their mechanism of action remains unknown. This review addresses the role of the metabolites produced by gut microbiota in cancer and obesity. It is clear that only if the link between microbial diversity and metabolic functionality is firmly established, will the mechanism by which gut microbiota maintains health or contributes to disease development be elucidated.

scholarly journals Differential Effects of Western and Mediterranean-Type Diets on Gut Microbiota: A Metagenomics and Metabolomics Approach

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2638
Author(s):  
Claudia Barber ◽  
Marianela Mego ◽  
Carlos Sabater ◽  
Fernando Vallejo ◽  
Rogger Alvaro Bendezu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Mediterranean Diet ◽  
Urinary Metabolites ◽  
Microbial Metabolism ◽  
Randomised Study ◽  
Metabolic Functions ◽  
Faecal Samples ◽  
Metabolite Profiles ◽  
Diet Versus ◽  
Colonic Content

Our aim was to determine the effect of diet on gut microbiota, digestive function and sensations, using an integrated clinical, metagenomics and metabolomics approach. We conducted a cross-over, randomised study on the effects of a Western-type diet versus a fibre-enriched Mediterranean diet. In 20 healthy men, each diet was administered for 2 weeks preceded by a 2-week washout diet. The following outcomes were recorded: (a) number of anal gas evacuations; (b) digestive sensations; (c) volume of gas evacuated after a probe meal; (d) colonic content by magnetic resonance imaging; (e) gut microbiota taxonomy and metabolic functions by shotgun sequencing of faecal samples; (f) urinary metabolites using untargeted metabolomics. As compared to a Western diet, the Mediterranean diet was associated with (i) higher number of anal gas evacuations, (ii) sensation of flatulence and borborygmi, (iii) larger volume of gas after the meal and (iv) larger colonic content. Despite the relatively little difference in microbiota composition between both diets, microbial metabolism differed substantially, as shown by urinary metabolite profiles and the abundance of microbial metabolic pathways. The effects of the diet were less evident in individuals with robust microbiotas (higher beta-diversity). To conclude, healthy individuals tolerate dietary changes with minor microbial modifications at the composition level but with remarkable variation in microbial metabolism.

Fecal microbial metabolism of polyphenols and its effects on human gut microbiota

Anaerobe ◽  
2013 ◽  
Vol 23 ◽  
pp. 12-19 ◽  
Author(s):  
Shanthi G. Parkar ◽  
Tania M. Trower ◽  
David E. Stevenson
Keyword(s):  
Gut Microbiota ◽  
Microbial Metabolism ◽  
Human Gut ◽  
Human Gut Microbiota

scholarly journals Genetic and Transcriptional Analysis of Human Host Response to Healthy Gut Microbiota

mSystems ◽  
2016 ◽  
Vol 1 (4) ◽  
Author(s):  
Allison L. Richards ◽  
Michael B. Burns ◽  
Adnan Alazizi ◽  
Luis B. Barreiro ◽  
Roger Pique-Regi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Gut Microbiota ◽  
Microbial Communities ◽  
Genotypic Variation ◽  
Experimental System ◽  
Host Genotype ◽  
Specific Expression ◽  
Colonic Epithelial Cells ◽  
Novel Approach ◽  
Transcriptional Changes

ABSTRACT The study of host-microbiota interactions in humans is largely limited to identifying associations between microbial communities and host phenotypes. While these studies have generated important insights on the links between the microbiota and human disease, the assessment of cause-and-effect relationships has been challenging. Although this relationship can be studied in germfree mice, this system is costly, and it is difficult to accurately account for the effects of host genotypic variation and environmental effects seen in humans. Here, we have developed a novel approach to directly investigate the transcriptional changes induced by live microbial communities on human colonic epithelial cells and how these changes are modulated by host genotype. This method is easily scalable to large numbers of host genetic backgrounds and diverse microbiota and can be utilized to elucidate the mechanisms of host-microbiota interactions. Future extensions may also include colonic organoid cultures. Many studies have demonstrated the importance of the gut microbiota in healthy and disease states. However, establishing the causality of host-microbiota interactions in humans is still challenging. Here, we describe a novel experimental system to define the transcriptional response induced by the microbiota for human cells and to shed light on the molecular mechanisms underlying host-gut microbiota interactions. In primary human colonic epithelial cells, we identified over 6,000 genes whose expression changed at various time points following coculturing with the gut microbiota of a healthy individual. Among the differentially expressed genes we found a 1.8-fold enrichment of genes associated with diseases that have been previously linked to the microbiome, such as obesity and colorectal cancer. In addition, our experimental system allowed us to identify 87 host single nucleotide polymorphisms (SNPs) that show allele-specific expression in 69 genes. Furthermore, for 12 SNPs in 12 different genes, allele-specific expression is conditional on the exposure to the microbiota. Of these 12 genes, 8 have been associated with diseases linked to the gut microbiota, specifically colorectal cancer, obesity, and type 2 diabetes. Our study demonstrates a scalable approach to study host-gut microbiota interactions and can be used to identify putative mechanisms for the interplay between host genetics and the microbiota in health and disease. IMPORTANCE The study of host-microbiota interactions in humans is largely limited to identifying associations between microbial communities and host phenotypes. While these studies have generated important insights on the links between the microbiota and human disease, the assessment of cause-and-effect relationships has been challenging. Although this relationship can be studied in germfree mice, this system is costly, and it is difficult to accurately account for the effects of host genotypic variation and environmental effects seen in humans. Here, we have developed a novel approach to directly investigate the transcriptional changes induced by live microbial communities on human colonic epithelial cells and how these changes are modulated by host genotype. This method is easily scalable to large numbers of host genetic backgrounds and diverse microbiota and can be utilized to elucidate the mechanisms of host-microbiota interactions. Future extensions may also include colonic organoid cultures.

scholarly journals Effects of GABA Supplementation on Intestinal SIgA Secretion and Gut Microbiota in the Healthy and ETEC-Infected Weanling Piglets

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Yuanyuan Zhao ◽  
Jing Wang ◽  
Hao Wang ◽  
Yonggang Huang ◽  
Ming Qi ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Immunoglobulin A ◽  
Public Health Problem ◽  
Enrichment Analysis ◽  
Basal Diet ◽  
Microbial Metabolism ◽  
Sphingolipid Metabolism ◽  
Weanling Piglets ◽  
Weaning Piglets ◽  
Two Stages

Pathogenic enterotoxigenic Escherichia coli (ETEC) has been considered a major cause of diarrhea which is a serious public health problem in humans and animals. This study was aimed at examining the effect of γ-aminobutyric acid (GABA) supplementation on intestinal secretory immunoglobulin A (SIgA) secretion and gut microbiota profile in healthy and ETEC-infected weaning piglets. A total of thirty-seven weaning piglets were randomly distributed into two groups fed with the basal diet or supplemented with 40 mg·kg−1 of GABA for three weeks, and some piglets were infected with ETEC at the last week. According to whether ETEC was inoculated or not, the experiment was divided into two stages (referred as CON1 and CON2 and GABA1 and GABA2). The growth performance, organ indices, amino acid levels, and biochemical parameters of serum, intestinal SIgA concentration, gut microbiota composition, and intestinal metabolites were analyzed at the end of each stage. We found that, in both the normal and ETEC-infected piglets, jejunal SIgA secretion and expression of some cytokines, such as IL-4, IL-13, and IL-17, were increased by GABA supplementation. Meanwhile, we observed that some low-abundance microbes, like Enterococcus and Bacteroidetes, were markedly increased in GABA-supplemented groups. KEGG enrichment analysis revealed that the nitrogen metabolism, sphingolipid signaling pathway, sphingolipid metabolism, and microbial metabolism in diverse environments were enriched in the GABA1 group. Further analysis revealed that alterations in microbial metabolism were closely correlated to changes in the abundances of Enterococcus and Bacteroidetes. In conclusion, GABA supplementation can enhance intestinal mucosal immunity by promoting jejunal SIgA secretion, which might be related with the T-cell-dependent pathway and altered gut microbiota structure and metabolism.

scholarly journals High fat diet induces microbiota-dependent silencing of enteroendocrine cells

2019 ◽  
Author(s):  
Lihua Ye ◽  
Olaf Mueller ◽  
Jennifer Bagwell ◽  
Michel Bagnat ◽  
Rodger A. Liddle ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Experimental System ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Sensory Cells ◽  
High Fat ◽  
Fat Feeding

ABSTRACTEnteroendocrine cells (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient information. Consumption of dietary fat contributes to metabolic disorders, but EEC adaptations to high fat feeding were unknown. Here, we established a new experimental system to directly investigate EEC activity in vivo using a zebrafish reporter of EEC calcium signaling. Our results reveal that high fat feeding alters EEC morphology and converts them into a nutrient insensitive state that is coupled to endoplasmic reticulum (ER) stress. We called this novel adaptation “EEC silencing”. Gnotobiotic studies revealed that germ-free zebrafish are resistant to high fat diet induced EEC silencing. High fat feeding altered gut microbiota composition including enrichment ofAcinetobacterspecies, and we identified anAcinetobacterstrain sufficient to induce EEC silencing. These results establish a new mechanism by which dietary fat and gut microbiota modulate EEC nutrient sensing and signaling.

Pepsin egg white hydrolysate modulates gut microbiota in Zucker obese rats

2017 ◽  
Vol 8 (1) ◽  
pp. 437-443 ◽  
Author(s):  
Teresa Requena ◽  
Marta Miguel ◽  
Marta Garcés-Rimón ◽  
M. Carmen Martínez-Cuesta ◽  
Rosina López-Fandiño ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Microbial Metabolism ◽  
Egg White ◽  
Obese Rats

Pepsin egg white hydrolysate favours lean-associated microbiota and microbial metabolism.

scholarly journals Interaction of dietary polyphenols and gut microbiota: Microbial metabolism of polyphenols, influence on the gut microbiota, and implications on host health

2020 ◽  
Vol 1 (2) ◽  
pp. 109-133 ◽  
Author(s):  
Gizem Catalkaya ◽  
Koen Venema ◽  
Luigi Lucini ◽  
Gabriele Rocchetti ◽  
Dominique Delmas ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Microbial Metabolism ◽  
Dietary Polyphenols ◽  
Host Health

scholarly journals High fat diet induces microbiota-dependent silencing of enteroendocrine cells

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Lihua Ye ◽  
Olaf Mueller ◽  
Jennifer Bagwell ◽  
Michel Bagnat ◽  
Rodger A Liddle ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Experimental System ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Sensory Cells ◽  
High Fat ◽  
Fat Feeding

Enteroendocrine cells (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient information. Consumption of dietary fat contributes to metabolic disorders, but EEC adaptations to high fat feeding were unknown. Here, we established a new experimental system to directly investigate EEC activity in vivo using a zebrafish reporter of EEC calcium signaling. Our results reveal that high fat feeding alters EEC morphology and converts them into a nutrient insensitive state that is coupled to endoplasmic reticulum (ER) stress. We called this novel adaptation 'EEC silencing'. Gnotobiotic studies revealed that germ-free zebrafish are resistant to high fat diet induced EEC silencing. High fat feeding altered gut microbiota composition including enrichment of Acinetobacter bacteria, and we identified an Acinetobacter strain sufficient to induce EEC silencing. These results establish a new mechanism by which dietary fat and gut microbiota modulate EEC nutrient sensing and signaling.

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