scholarly journals Preterm infant gut microbiota affects intestinal epithelial development in a humanized microbiome gnotobiotic mouse model

2016 ◽  
Vol 311 (3) ◽  
pp. G521-G532 ◽  
Author(s):  
Yueyue Yu ◽  
Lei Lu ◽  
Jun Sun ◽  
Elaine O. Petrof ◽  
Erika C. Claud
Keyword(s):  
Weight Gain ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Preterm Infant ◽  
Microbial Communities ◽  
Goblet Cells ◽  
Paneth Cells ◽  
Stem Cell Marker ◽  
Intestinal Development ◽  
The Impact

Development of the infant small intestine is influenced by bacterial colonization. To promote establishment of optimal microbial communities in preterm infants, knowledge of the beneficial functions of the early gut microbiota on intestinal development is needed. The purpose of this study was to investigate the impact of early preterm infant microbiota on host gut development using a gnotobiotic mouse model. Histological assessment of intestinal development was performed. The differentiation of four epithelial cell lineages (enterocytes, goblet cells, Paneth cells, enteroendocrine cells) and tight junction (TJ) formation was examined. Using weight gain as a surrogate marker for health, we found that early microbiota from a preterm infant with normal weight gain (MPI-H) induced increased villus height and crypt depth, increased cell proliferation, increased numbers of goblet cells and Paneth cells, and enhanced TJs compared with the changes induced by early microbiota from a poor weight gain preterm infant (MPI-L). Laser capture microdissection (LCM) plus qRT-PCR further revealed, in MPI-H mice, a higher expression of stem cell marker Lgr5 and Paneth cell markers Lyz1 and Cryptdin5 in crypt populations, along with higher expression of the goblet cell and mature enterocyte marker Muc3 in villus populations. In contrast, MPI-L microbiota failed to induce the aforementioned changes and presented intestinal characteristics comparable to a germ-free host. Our data demonstrate that microbial communities have differential effects on intestinal development. Future studies to identify pioneer settlers in neonatal microbial communities necessary to induce maturation may provide new insights for preterm infant microbial ecosystem therapeutics.

scholarly journals The Application of Metabolomics to Probiotic and Prebiotic Interventions in Human Clinical Studies

Metabolites ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 120
Author(s):  
Thomas M. O’Connell
Keyword(s):  
Clinical Trials ◽  
Nucleic Acid ◽  
Gut Microbiota ◽  
Microbial Communities ◽  
Biochemical Mechanism ◽  
Beneficial Bacteria ◽  
Future Studies ◽  
Current State ◽  
Live Bacteria ◽  
The Impact

There is an ever-increasing appreciation for our gut microbiota that plays a crucial role in the maintenance of health, as well as the development of disease. Probiotics are live bacteria that are consumed to increase the population of beneficial bacteria and prebiotics are dietary substrates intended to promote the propagation of beneficial bacteria. In order to optimize the use of probiotics and prebiotics, a more complete biochemical understanding of the impact that these treatments have on the community and functioning of the gut microbiota is required. Nucleic acid sequencing methods can provide highly detailed information on the composition of the microbial communities but provide less information on the actual function. As bacteria impart much of their influence on the host through the production of metabolites, there is much to be learned by the application of metabolomics. The focus of this review is on the use of metabolomics in the study of probiotic and prebiotic treatments in the context of human clinical trials. Assessment of the current state of this research will help guide the design of future studies to further elucidate the biochemical mechanism by which probiotics and prebiotics function and pave the way toward more personalized applications.

scholarly journals Synbiotic Supplementation Modulates Gut Microbiota, Regulates Beta-Catenin Expression And Prevents Weight Gain in ob/ob Mice

2021 ◽  
Author(s):  
Sebastião Mauro Bezerra Duarte ◽  
José Tadeu Stefano ◽  
Lucas A. M. Franco ◽  
Roberta C. Martins ◽  
Bruna D. G. C. Moraes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Body Weight Gain ◽  
Standard Diet ◽  
Beta Catenin ◽  
Reduced Body ◽  
Synbiotic Supplementation ◽  
And Control ◽  
The Impact

Abstract Background: The aim of this study was to examine the impact of synbiotic supplementation in obesity and microbiota in ob/ob mice. 20 animals were divided into four groups: Obese Treated (OT), Control (OC), Lean Treated (LT) and Control (LC). All animals received standard diet for 8 weeks. Treated groups received a synbiotic in water while nontreated groups received water. After 8 weeks, all animals were sacrificed and gut tissue mRNA isolation and stool samples by microbiota analysis were collected. Beta-catenin, occludin, cadherin and zonulin were analyzed in gut tissue by RT-qPCR. Results: The synbiotic supplementation reduced body weight gain in OT comparing with OC (p=0.0398), increase of Enterobacteriaceae (p=0.005) and decrease of Cyanobacteria (p=0.047), Clostridiaceae (p=0.026), Turicibacterales (p=0.005) and Coprococcus (p=0.047). A significant reduction of Sutterella bacteria (p=0.009) and Turicibacter (p=0.005) was observed in LT compared to LC. Alpha and beta diversities were differ between all treated groups. Beta-catenin gene expression was significantly decreased in the gut tissue of OT (p≤0.0001) when compared to other groups. No changes were observed in occludin, cadherin and zonulin gene expression in the gut tissue. Conclusion: The synbiotics supplementation prevents excessive weight gain, modulates the gut microbiota, and reduces beta-catenin expression in ob/ob mice.

scholarly journals High-Fructose Diet Alters Intestinal Microbial Profile and Correlates with Early Tumorigenesis in a Mouse Model of Barrett’s Esophagus

2021 ◽  
Vol 9 (12) ◽  
pp. 2432
Author(s):  
Andrea Proaño-Vasco ◽  
Theresa Baumeister ◽  
Amira Metwaly ◽  
Sandra Reitmeier ◽  
Karin Kleigrewe ◽  
...  
Keyword(s):  
Mouse Model ◽  
Gut Microbiota ◽  
Microbial Communities ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Industrialized Countries ◽  
High Fructose Diet ◽  
Microbial Profile ◽  
High Fructose ◽  
Colon Cancer Cell Lines

Esophageal adenocarcinoma (EAC) is mostly prevalent in industrialized countries and has been associated with obesity, commonly linked with a diet rich in fat and refined sugars containing high fructose concentrations. In meta-organisms, dietary components are digested and metabolized by the host and its gut microbiota. Fructose has been shown to induce proliferation and cell growth in pancreas and colon cancer cell lines and also alter the gut microbiota. In a previous study with the L2-IL-1B mouse model, we showed that a high-fat diet (HFD) accelerated EAC progression from its precursor lesion Barrett’s esophagus (BE) through changes in the gut microbiota. Aiming to investigate whether a high-fructose diet (HFrD) also alters the gut microbiota and favors EAC carcinogenesis, we assessed the effects of HFrD on the phenotype and intestinal microbial communities of L2-IL1B mice. Results showed a moderate acceleration in histologic disease progression, a mild effect on the systemic inflammatory response, metabolic changes in the host, and a shift in the composition, metabolism, and functionality of intestinal microbial communities. We conclude that HFrD alters the overall balance of the gut microbiota and induces an acceleration in EAC progression in a less pronounced manner than HFD.

scholarly journals Fluoxetine-induced alteration of murine gut microbial community structure: evidence for a microbial endocrinology-based mechanism of action responsible for fluoxetine-induced side effects

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6199 ◽  
Author(s):  
Mark Lyte ◽  
Karrie M. Daniels ◽  
Stephan Schmitz-Esser
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Side Effects ◽  
Gut Microbiota ◽  
Microbial Communities ◽  
Time Course ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Sequence Data ◽  
Rrna Gene ◽  
Dosing Regimen

Background Depression and major depressive disorder affect 25% of the population. First line treatment utilizing selective serotonin reuptake inhibitors (SSRIs) have met with limited success due to well-recognized negative side effects which include weight gain or loss. This inability to control unwanted side effects often result in patients stopping their antidepressant medications. The mechanisms underlying the failure of SSRIs are incompletely understood. Methods Male CF-1 mice (5 weeks of age, N = 10 per group) were per orally administered fluoxetine (20 mg per kg body weight) or diluent daily for 29 days. During this time fecal specimens were collected at three defined time points (0, 15 and 29 days). At the conclusion of the 29-day dosing regimen, animals were subjected to two behavioral assessments. For bacterial identification of the microbiota, 16S rRNA gene sequencing was performed on 60 fecal specimens (three specimens per mouse time course, N = 20 mice) using Illumina MiSeq. Analysis of community sequence data was done using mothur and LEfSe bioinformatic software packages. Results Daily per oral administration of fluoxetine for 29 days to male mice resulted in a significant, time dependent, alteration in microbial communities accompanying changes in body weight. The calculated species richness and diversity indicators of the murine fecal microbial communities were inconsistent and not significantly different between the groups. Among the phylotypes decreased in abundance due to fluoxetine administration were Lactobacillus johnsonii and Bacteroidales S24-7 which belong to phyla associated with regulation of body mass. The observed changes in body weight due to fluoxetine administration mimicked the dramatic shifts in weight gain/loss that has been observed in humans. Further, at the conclusion of the 29-day dosing regimen fluoxetine-dosed animals evidenced a mild anxiogenic-like behavior. Discussion We report that the most widely used antidepressant, fluoxetine, which is an SSRI-type drug, results in the selective depletion of gut microbiota, specifically the Lactobacilli which are involved in the regulation of body weight. Concomitantly, fluoxetine administration increases the abundance of phylotypes related to dysbiosis. Since Lactobacilli have been previously shown to possess a known biogenic amine transporter that regulates the uptake of fluoxetine, it is proposed that a microbial endocrinology-based mechanistic pathway is responsible for the ability of SSRIs to selectively negatively impact beneficial microbiota. The results of this study therefore suggest that the negative clinical side effects due to fluoxetine administration may be due to alterations in gut microbiota. Further, the data also suggests that supplementation of bacterial genera directly affected by fluoxetine administration may prove useful in ameliorating some of the well-known side effects of chronic fluoxetine administration such as weight alterations.

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 Synbiotic Supplementation Modulates Gut Microbiota, Regulates Beta-catenin Expression and Prevents Weight Gain in Ob/ob Mice

2021 ◽  
Author(s):  
Sebastião Mauro Bezerra Duarte ◽  
José Tadeu Stefano ◽  
Lucas A. M. Franco ◽  
Roberta C. Martins ◽  
Bruna D. G. C. Moraes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Body Weight Gain ◽  
Standard Diet ◽  
Beta Catenin ◽  
Stool Samples ◽  
Synbiotic Supplementation ◽  
And Control ◽  
The Impact

Abstract Background: Obesity is one of the main health problems in the world today and dysbiosis seem to be one of the factors involved. The aim of this study was to examine the impact of synbiotic supplementation in obesity and microbiota in ob/ob mice. 20 animals were divided into four groups: Obese Treated (OT) and Control (OC), Lean Treated (LT) and Control (LC). All animals received standard diet for 8 weeks. Treated groups received a synbiotic in water while nontreated groups received water. After 8 weeks, all animals were sacrificed and gut tissue mRNA isolation and stool samples by microbiota analysis were collected. Beta-catenin, occludin, cadherin and zonulin were analyzed in gut tissue by RT-qPCR. Microbiome DNA was extracted from stool samples and sequenced using the Ion PGM Torrent platform. Results: The synbiotic supplementation reduced body weight gain in OT group comparing with OC (p=0.0398), increase of Enterobacteriaceae (p=0.005) and decrease of Cyanobacteria (p=0.047), Clostridiaceae (p=0.026), Turicibacterales (p=0.005) and Coprococcus (p=0.047). In the other hand, a significant reduction of Sutterella bacteria (p=0.009) and Turicibacter (p=0.005) was observed in LT group compared to LC. Alpha and beta diversities were differ between all treated groups. Beta-catenin gene expression was significantly decreased in the gut tissue of OT group (p≤0.0001) when compared to other groups. No changes were observed in occludin, cadherin and zonulin gene expression in the gut tissue. Conclusion: The synbiotics supplementation prevents excessive weight gain, modulates the gut microbiota, and reduces beta-catenin expression in ob/ob mice.

scholarly journals Evaluation of 2’-Fucosyllactose and Bifidobacterium longum Subspecies infantis on Growth, Organ Weights, and Intestinal Development of Piglets

Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 199
Author(s):  
Victoria C. Daniels ◽  
Marcia H. Monaco ◽  
Mei Wang ◽  
Johanna Hirvonen ◽  
Henrik Max Jensen ◽  
...  
Keyword(s):  
Weight Gain ◽  
Infant Development ◽  
Body Weight Gain ◽  
Bifidobacterium Longum ◽  
Total Body Weight ◽  
Milk Replacer ◽  
Intestinal Development ◽  
Organ Weights ◽  
Body Weights ◽  
The Impact

Human milk is rich in oligosaccharides that influence intestinal development and serve as prebiotics for the infant gut microbiota. Probiotics and 2’-fucosyllactose (2’-FL) added individually to infant formula have been shown to influence infant development, but less is known about the effects of their synbiotic administration. Herein, the impact of formula supplementation with 2’-fucosyllactose (2’-FL) and Bifidobacterium longum subsp. infantis Bi-26 (Bi-26), or 2’-FL + Bi-26 on weight gain, organ weights, and intestinal development in piglets was investigated. Two-day-old piglets (n = 53) were randomized in a 2 × 2 design to be fed a commercial milk replacer ad libitum without (CON) or with 1.0 g/L 2’-FL. Piglets in each diet were further randomized to receive either glycerol stock alone or Bi-26 (109 CFU) orally once daily. Body weights and food intake were monitored from postnatal day (PND) 2 to 33/34. On PND 34/35, animals were euthanized and intestine, liver and brain weights were assessed. Intestinal samples were collected for morphological analyses and measurement of disaccharidase activity. Dry matter of cecum and colon contents and Bifidobacterium longum subsp. infantis abundance by RT-PCR were also measured. All diets were well tolerated, and formula intake did not differ among the treatment groups. Daily body weights were affected by 2’-FL, Bi-26, and day, but no interaction was observed. There was a trend (p = 0.075) for greater total body weight gain in CON versus all other groups. Jejunal and ascending colon histomorphology were unaffected by treatment; however, there were main effects of 2’-FL to increase (p = 0.040) and Bi-26 to decrease (p = 0.001) ileal crypt depth. The addition of 2’-FL and/or Bi-26 to milk replacer supported piglet growth with no detrimental effects on body and organ weights, or intestinal structure and function.

Dysregulated microbiota-gut-brain axis

2017 ◽  
Vol 47 (5) ◽  
pp. 648-658 ◽  
Author(s):  
Arbind Kumar Choudhary ◽  
Yeong Lee
Keyword(s):  
Weight Gain ◽  
Side Effects ◽  
Gut Microbiota ◽  
Metabolic Effects ◽  
Health Concern ◽  
Metabolic Dysfunction ◽  
Content Type ◽  
Glucose Levels ◽  
Gut Dysbiosis ◽  
The Impact

Purpose This paper aims to summarize the available literatures, specifically in the following areas: metabolic and other side effects of aspartame; microbiota changes/dysbiosis and its effect on the gut-brain axis; changes on gut microbiota as a result of aspartame usage; metabolic effects (weight gain and glucose intolerance) of aspartame due to gut dysbiosis; and postulated effects of dysregulated microbiota-gut-brain axis on other aspartame side-effects (neurophysiological symptoms and immune dysfunction). Design/methodology/approach Aspartame is rapidly becoming a public health concern because of its purported side-effects especially neurophysiological symptom and immune dysregulation. It is also paradoxical that metabolic consequences including weight gain and impaired blood glucose levels have been observed in consumers. Exact mechanisms of above side-effects are unclear, and data are scarce but aspartame, and its metabolites may have caused disturbance in the microbiota-gut-brain axis. Findings Additional studies investigating the impact of aspartame on gut microbiota and metabolic health are needed. Originality/value Exact mechanism by which aspartame-induced gut dysbiosis and metabolic dysfunction requires further investigation.

scholarly journals Exercise Prevents Weight Gain and Alters the Gut Microbiota in a Mouse Model of High Fat Diet-Induced Obesity

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e92193 ◽  
Author(s):  
Christian C. Evans ◽  
Kathy J. LePard ◽  
Jeff W. Kwak ◽  
Mary C. Stancukas ◽  
Samantha Laskowski ◽  
...  
Keyword(s):  
Weight Gain ◽  
Mouse Model ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Evaluation of Poorly-Bioavailable Cocoa Flavanols and Their Gut Microbial Metabolites in Potentiating Anti-diabetic Activities Through BTBR.Cg-Lepob/ob/WiscJ Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 361-361
Author(s):  
Kathryn Racine ◽  
Lisard Iglesias-Carres ◽  
Lauren Essenmacher ◽  
Gabriella Agnello ◽  
Jeffery Tessem ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Significant Protection ◽  
Peripheral Tissues ◽  
Progressive Type ◽  
Males And Females ◽  
The Impact ◽  
Cocoa Flavanols

Abstract Objectives Cocoa (Theobroma cacao) is a concentrated dietary source of flavanols that have beneficial activities against type-2 diabetes. These compounds have limited small intestinal absorption and are metabolized by the microbiota to bioavailable metabolites that may exert anti-diabetic effects locally and in peripheral tissues. Our objectives were to 1) determine the role of the gut microbiome in facilitating protective effects of cocoa flavanols, and 2) evaluate these effects in a novel mouse model of progressive type-2 diabetes. Methods A small pilot study (n = 3) of male and female BTBR mice (wild-type and homozygous for the Lepob mutation) received either control or cocoa extract-supplemented diet for 10 weeks. Half the animals were administered antibiotics orally to knock down the commensal gut microbiota. Glucose and insulin tolerance tests were conducted at weeks 1 and 5 and 2 and 6, respectively. Weight gain and food intake were monitored weekly. Biomarkers of gut integrity and inflammation were assessed by ELISA. Results Baseline fasting blood glucose (FBG) levels in five-week-old homozygous males and females were measured at 211–271 mg/dL and 112–234 mg/dL, respectively. After five weeks, FBG measured at 281–438 mg/dL and 177–562 mg/dL, respectively. Cocoa provided moderate, yet not significant, protection against weight gain in homozygous males when compared to homozygous males fed control diet. Cocoa provided no significant protection against hypoglycemia in homozygous male or female mice when compared to homozygous controls. In treatment comparisons with and without antibiotics, knocking out the commensal gut microbiota appeared to have minimal effect on weight gain and glycemic control in both males and females. Conclusions Cocoa did provide a moderate level of protection for homozygous males when directly comparing weight gain and FBG across sex. While the microbiome has displayed a promising role in the bioavailability of large flavanols, in this particular model, the impact was minimal. Overall, cocoa was ineffective against the mediation of advanced diabetes and further work must be conducted to understand if this conclusion is isolated to this model of progressive type-2 diabetes. Funding Sources This work was supported by the US Department of Agriculture by AFRI grant 2020–67,017-30,846.

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