scholarly journals Fluoride Induced Leaky Gut and Bloom of Erysipelatoclostridium Ramosum Mediate the Exacerbation of Obesity in High-Fat-Diet Fed Mice

2021 ◽  
Author(s):  
Guijie Chen ◽  
Yujia Peng ◽  
Yujie Huang ◽  
Minhao Xie ◽  
Zhuqing Dai ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Fecal Microbiota Transplantation ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
Normal Diet ◽  
High Fat ◽  
Strong Relation ◽  
Potential Strategy ◽  
Treatment Of Obesity

Abstract Background: Fluoride, a necessary mineral element for our health, is widely presented in drinking water and foods. The intake of excessive fluoride showed potential risk to human health. A strong relation between fluoride exposure and obesity has been reported. However, the knowledge on the potential mechanisms on fluoride-induced obesity is still limited.Results: In this work, we showed here that fluoride alone did not induce obesity in normal diet fed mice, whereas, it could trigger exacerbation of obesity in high-fat diet (HFD) fed mice. Fluoride impaired intestinal barrier and activated Toll-like receptor 4 (TLR4) signaling to induce obesity, which was further verified in TLR4-/- mice. Furthermore, fluoride could deteriorate the gut microbiota in HFD mice. The fecal microbiota transplantation from fluoride-induced mice was sufficient to induce obesity, while the exacerbation of obesity by fluoride was blocked upon gut microbiota depletion. The fluoride-induced bloom of Erysipelatoclostridium ramosum belonged to Erysipelotrichaceae was responsible for exacerbation of obesity. In addition, a potential strategy for prevention of fluoride-induced obesity was proposed by intervention with polysaccharides from Fuzhuan brick tea.Conclusions: Overall, these results provide the first evidence of a comprehensive cross-talk mechanism between fluoride and obesity in HFD fed mice, which is mediated by gut microbiota and intestinal barrier. E. ramosum was identified as a crucial mediator of fluoride induced obesity, which could be explored as potential target for prevention and treatment of obesity with exciting translational value.

scholarly journals Obesity-induced gut microbiota dysbiosis can be ameliorated by fecal microbiota transplantation: a multiomics approach

2019 ◽  
Author(s):  
Maria Guirro ◽  
Andrea Costa ◽  
Andreu Gual-Grau ◽  
Pol Herrero ◽  
Helena Torrell ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Fecal Microbiota Transplantation ◽  
Obese Subject ◽  
Fecal Microbiota ◽  
Obesity Therapy ◽  
Treatment Of Obesity ◽  
And Function ◽  
Hypercaloric Diet ◽  
Gut Microbiota Dysbiosis

AbstractObesity and its comorbidities are currently considered an epidemic, and the involved pathophysiology is well studied. Recently, the gut microbiota has emerged as a new potential therapeutic target for the treatment of obesity. Diet and antibiotics are known to play crucial roles in changes in the microbiota ecosystem and the disruption of its balance; therefore, the manipulation of gut microbiota may represent a strategy for obesity treatment. Fecal microbiota transplantation, during which fecal microbiota from a healthy donor is transplanted to an obese subject, has aroused interest as an effective approach for the treatment of obesity. To determine its success, a multiomics approach was used that combined metagenomics and metaproteomics to study microbiota composition and function.To do this, a study was performed in rats that evaluated the effect of a hypercaloric diet on the gut microbiota, and this was combined with antibiotic treatment to deplete the microbiota before fecal microbiota transplantation to verify its effects on gut microbiota-host homeostasis. Our results showed that a high-fat diet induces changes in microbiota biodiversity and alters its function in the host. Moreover, we found that antibiotics depleted the microbiota enough to reduce its bacterial content. Finally, we assessed the use of fecal microbiota transplantation as an obesity therapy, and we found that it reversed the effects of antibiotics and reestablished the microbiota balance, which restored normal functioning and alleviated microbiota disruption.

scholarly journals Sugar-sweetened Beverage and High Fat Diet Consumption Harmfully Alters Gut Microbiota and Promotes Gut Inflammation (P20-041-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Woo-Jeong Shon ◽  
Min Ho Jung ◽  
Eun Young Choi ◽  
Dong-Mi Shin
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Large Scale ◽  
Fecal Microbiota Transplantation ◽  
Critical Role ◽  
Science Research ◽  
Fecal Microbiota ◽  
Sugar Solution ◽  
High Fat ◽  
High Sugar

Abstract Objectives It is clear that epidemiologic trends document a dramatic increasing incidence of inflammatory bowel disease (IBD) paralleling global westernization. Despite strong tie among diets, gut microbiota (GM) and IBD, the exact mechanisms causing IBD remains incompletely understood. Here we hypothesized that changes in the gut immune system, in response to changes in gut microbiome induced "Westernized diet", would be sufficient to trigger IBD. Methods We set out to test this hypothesized by analyzing the changes in gut microbiota composition induced by feeding mice with High sugar-solution or/and High fat and demonstrated their causal roles through high-throughput microbiome analyses. We further assessed changes in inflammatory cell recruitment using flow cytometry, and performed transcriptomic profiling analyses of intestine tissue to identify altered gut microbiota deliver changes in intestinal innate immune and adaptive T cell homeostasis. Importantly, to identify the role of the microbiota in directing host immune responses, fecal microbiota transplantation (FMT) experiments were conducted. Results The microbiome analyses results showed that Prevotella, Betaproteobacteria, and Cytophaga, which are a well-known the most representative species in IBD, was significantly enriched only in the HF-Sugar group, suggesting that addition of high-sugar to high-fat diet may reshape the GM by favoring colonization of pathobionts. Also, transcriptome and FACS profiling results showed, among others, high sugar synergistically changes intestinal transcriptomic signature related Inflammatory/Immune Response induced by several pro-inflammatory cytokines and induces expansion of inflammatory DCs and T cells driven by the high fat diet. By using FMT, we prove that host immune traits can be regulated by altering the GM. Conclusions Together, our large-scale profiling analyses may uncover an interaction between dietary alterations causing IBD and gut microbiota and provide helpful information regarding the microbiota plays a critical role in programming the immune phenotypes of the host. Funding Sources This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2018R1D1A1B07048023).

scholarly journals Insights into the Impact of Microbiota in the Treatment of NAFLD/NASH and Its Potential as a Biomarker for Prognosis and Diagnosis

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 145
Author(s):  
Julio Plaza-Díaz ◽  
Patricio Solis-Urra ◽  
Jerónimo Aragón-Vela ◽  
Fernando Rodríguez-Rodríguez ◽  
Jorge Olivares-Arancibia ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Liver Steatosis ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
Current Treatment ◽  
Immune Defense ◽  
Alcoholic Fatty Liver ◽  
The Impact

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

The ameliorative effect of the Pyracantha fortuneana (Maxim.) H. L. Li extract on intestinal barrier dysfunction through modulating glycolipid digestion and gut microbiota in high fat diet-fed rats

2019 ◽  
Vol 10 (10) ◽  
pp. 6517-6532 ◽  
Author(s):  
Hang Xu ◽  
Chunfang Zhao ◽  
Yutian Li ◽  
Ruiyu Liu ◽  
Mingzhang Ao ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Intestinal Barrier ◽  
High Fat ◽  
Barrier Dysfunction ◽  
Fruit Extract ◽  
Intestinal Barrier Dysfunction ◽  
Beneficial Effects ◽  
Obese Rats ◽  
Ameliorative Effect

Pyracantha fortuneana fruit extract (PFE) exhibits beneficial effects on IBF in association with the modulation of glycolipid digestion and gut microbiota in HFD-fed obese rats.

scholarly journals α-Methyl-L-Tryptophan as a Weight-Loss Agent in Multiple Models of Obesity in Mice

2021 ◽  
Author(s):  
Sathish Sivaprakasam ◽  
Sabarish Ramachandran ◽  
Mohd Omar Faruk Sikder ◽  
Yangzom Doma Bhutia ◽  
Mitchell Wachtel ◽  
...  
Keyword(s):  
Weight Loss ◽  
High Fat Diet ◽  
Amino Acid Profile ◽  
Normal Diet ◽  
The Body ◽  
Multiple Models ◽  
High Fat ◽  
Liver And Kidney ◽  
Obesity In Mice ◽  
Treatment Of Obesity

a-Methyl-L-tryptophan (a-MLT) is currently in use as a tracer in its 11C-labeled form to monitor the health of serotonergic neurons in humans. In the present study, we found this compound to function as an effective weight-loss agent at pharmacological doses in multiple models of obesity in mice. The drug was able to reduce the body weight when given orally in drinking water (1 mg/ml) in three different models of obesity: normal mice on high-fat diet, Slc6a14-null mice on high-fat diet, and ob/ob mice on normal diet. Only the L-enantiomer (a-MLT) was active while the D-enantiomer (a-MDT) had negligible activity. The weight-loss effect was freely reversible, with the weight gain resuming soon after the withdrawal of the drug. All three models of obesity were associated with hyperglycemia, insulin resistance, and hepatic steatosis; a-MLT reversed these features. There was a decrease in food intake in the treatment group. Mice on a high-fat diet showed decreased cholesterol and protein in the serum when treated with a-MLT; there was however no evidence of liver and kidney dysfunction. Plasma amino acid profile indicated a significant decrease in the levels of specific amino acids, including tryptophan; but the levels of arginine were increased. We conclude that a-MLT is an effective, reversible, and orally active drug for the treatment of obesity and metabolic syndrome.

scholarly journals Modulation of the Gut Microbiota by Shen-Yan-Fang-Shuai Formula Improves Obesity Induced by High-Fat Diets

2020 ◽  
Vol 11 ◽  
Author(s):  
Zhen Wang ◽  
Junfeng Lu ◽  
Jingwei Zhou ◽  
Weiwei Sun ◽  
Yang Qiu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
16S Rrna Genes ◽  
Rrna Genes ◽  
Therapeutic Effects ◽  
Low Grade ◽  
High Fat ◽  
Gut Barrier Function

Obesity and related metabolic disorders are associated with intestinal microbiota dysbiosis, disrupted intestinal barrier and chronic inflammation. Shen-Yan-Fang-Shuai formula (SYFSF) is a traditional Chinese herbal formula composed of Astragali Radix, Radix Angelicae Sinensis, Rheum Officinale Baill, and four other herbs. In this study, we identified that SYFSF treatment prevented weight gain, low-grade inflammation and insulin resistance in high-fat diet (HFD)-fed mice. SYFSF also substantially improved gut barrier function, reduced metabolic endotoxemia, as well as systemic inflammation. Sequencing of 16S rRNA genes obtained from fecal samples demonstrated that SYFSF attenuated HFD-induced gut dysbiosis, seen an decreased Firmicutes to Bacteroidetes ratios. Microbial richness and diversity were also higher in the SYFSF-treated HFD group. Furthermore, similar therapeutic effects and changes in gut microbiota profile caused by SYFSF could be replicated by fecal microbiota transfer (FMT). Taken together, our study highlights the efficacy of SYFSF in preventing obesity and related metabolic disorders. Its therapeutic effect is associated with the modulation of gut microbiota, as a prebiotic.

scholarly journals Glucosamine Ameliorates Symptoms of High-Fat Diet-Fed Mice by Reversing Imbalanced Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Xubing Yuan ◽  
Junping Zheng ◽  
Lishi Ren ◽  
Siming Jiao ◽  
Cui Feng ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Fasting Blood Glucose ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Rdna Sequencing

Glucosamine (GlcN) is used as a supplement for arthritis and joint pain and has been proved to have effects on inflammation, cancer, and cardiovascular diseases. However, there are limited studies on the regulatory mechanism of GlcN against glucose and lipid metabolism disorder. In this study, we treated high-fat diet (HFD)-induced diabetic mice with GlcN (1 mg/ml, in drinking water) for five months. The results show that GlcN significantly reduced the fasting blood glucose of HFD-fed mice and improved glucose tolerance. The feces of intestinal contents in mice were analyzed using 16s rDNA sequencing. It was indicated that GlcN reversed the imbalanced gut microbiota in HFD-fed mice. Based on the PICRUSt assay, the signaling pathways of glucolipid metabolism and biosynthesis were changed in mice with HFD feeding. By quantitative real-time PCR (qPCR) and hematoxylin and eosin (H&E) staining, it was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice. Finally, the correlation analysis suggests the most significantly changed intestinal bacteria were positively or negatively related to the occurrence of inflammation in the colon and fat tissues of HFD-fed mice. In summary, our studies provide a theoretical basis for the potential application of GlcN to glucolipid metabolism disorder through the regulation of gut microbiota.

scholarly journals Improvement of Colonic Immune Function with Soy Isoflavones in High-Fat Diet-Induced Obese Rats

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1139 ◽  
Author(s):  
Qihui Luo ◽  
Dongjing Cheng ◽  
Chao Huang ◽  
Yifan Li ◽  
Chengjie Lao ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Immune Function ◽  
Barrier Function ◽  
High Fat Diet ◽  
Intestinal Barrier ◽  
Soy Isoflavones ◽  
Short Chain ◽  
Intestinal Barrier Function ◽  
High Fat ◽  
Obese Rats

Background: The damage to intestinal barrier function plays an important role in the development of obesity and associated diseases. Soy isoflavones are effective natural active components for controlling obesity and reducing the level of blood lipid. Here, we explored whether these effects of soy isoflavones were associated with the intestinal barrier function. Methods and Results: The obese rat models were established by high fat diet feeding. Then, those obese rats were supplemented with soy isoflavones at different doses for 4 weeks. Our results showed that obesity induced the expressions of pro-inflammatory cytokines, decreased the anti-inflammatory cytokine (IL-10) expression, elevated intestinal permeability, altered gut microbiota and exacerbated oxidative damages in colon. The administration of soy isoflavones reversed these changes in obese rats, presenting as the improvement of intestinal immune function and permeability, attenuation of oxidative damage, increase in the fraction of beneficial bacteria producing short-chain fatty acids and short-chain fatty acid production, and reduction in harmful bacteria. Furthermore, soy isoflavones blocked the expressions of TLR4 and NF-κB in the colons of the obese rats. Conclusions: Soy isoflavones could improve obesity through the attenuation of intestinal oxidative stress, recovery of immune and mucosal barrier, as well as re-balance of intestinal gut microbiota.

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