Antimicrobial Emulsifier-Glycerol Monolaurate Induces Metabolic Syndrome, Gut Microbiota Dysbiosis, and Systemic Low-Grade Inflammation in Low-Fat Diet Fed Mice

2018 ◽  
Vol 62 (3) ◽  
pp. 1700547 ◽  
Author(s):  
Zengliang Jiang ◽  
Minjie Zhao ◽  
Hui Zhang ◽  
Yang Li ◽  
Mengyun Liu ◽  
...  
2021 ◽  
Author(s):  
Yang Liu ◽  
Wei Xiao ◽  
Leilei Yu ◽  
Fengwei Tian ◽  
Gang Wang ◽  
...  

Irritable bowel syndrome (IBS) is a chronic intestinal disorder accompanied by low-grade inflammation, visceral hypersensitivity, and gut microbiota dysbiosis. Several studies have indicated that Lactobacillus supplementation can help to alleviate...


2019 ◽  
Vol 317 (6) ◽  
pp. E1121-E1130 ◽  
Author(s):  
Aneseh Adeshirlarijaney ◽  
Jun Zou ◽  
Hao Q. Tran ◽  
Benoit Chassaing ◽  
Andrew T. Gewirtz

Metformin beneficially impacts several aspects of metabolic syndrome including dysglycemia, obesity, and liver dysfunction, thus making it a widely used frontline treatment for early-stage type 2 diabetes, which is associated with these disorders. Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota. In accord with this possibility, we observed herein that, in mice with diet-induced metabolic syndrome, metformin impacts the gut microbiota by preventing its encroachment upon the host, a feature of metabolic syndrome in mice and humans. However, the ability of metformin to beneficially impact metabolic syndrome in mice was not markedly altered by reduction or elimination of gut microbiota, achieved by the use of antibiotics or germfree mice. Although reducing or eliminating microbiota by itself suppressed diet-induced dysglycemia, other features of metabolic syndrome including obesity, hepatic steatosis, and low-grade inflammation remained suppressed by metformin in the presence or absence of gut microbiota. These results support a role for anti-inflammatory activity of metformin, irrespective of gut microbiota, in driving some of the beneficial impacts of this drug on metabolic syndrome.


2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Simona Mihai ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Ana-Maria Enciu ◽  
Lucian Albulescu ◽  
...  

Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.


2013 ◽  
Vol 42 (1) ◽  
pp. 49-53 ◽  
Author(s):  
Benoit Chassaing ◽  
Andrew T. Gewirtz

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1651 ◽  
Author(s):  
Alice Chaplin ◽  
Christian Carpéné ◽  
Josep Mercader

Resveratrol is a polyphenol which has been shown to have beneficial effects on metabolic syndrome-related alterations in experimental animals, including glucose and lipid homeostasis improvement and a reduction in fat mass, blood pressure, low-grade inflammation, and oxidative stress. Clinical trials have been carried out to address its potential; however, results are still inconclusive. Even though resveratrol is partly metabolized by gut microbiota, the relevance of this “forgotten organ” had not been widely considered. However, in the past few years, data has emerged suggesting that the therapeutic potential of this compound may be due to its interaction with gut microbiota, reporting changes in bacterial composition associated with beneficial metabolic outcomes. Even though data is still scarce and for the most part observational, it is promising nevertheless, suggesting that resveratrol supplementation could be a useful tool for the treatment of metabolic syndrome and its associated conditions.


2018 ◽  
Author(s):  
CHEN YanPingf ◽  
LIAO Tao ◽  
TAN LiLi ◽  
CHEN DongMei ◽  
XU Qin ◽  
...  

AbstractBy gut microbiota metagenomic analysis, we found that the abundance of sulfatase-secreting bacteria (SSB) in the gut of mice fed chondroitin sulfate (CS) increases with significant individual difference. The fluctuation of lipopolysaccharide (LPS) and pro-inflammatory indicators with significant individual and tissue variations was also observed. After mice were fed mixed with CS or injected separately with LPS, the breast cancer-related transcriptional factor genes, BCL11A and RUNX1, were upregulated, whereas the tumor suppressor gene, TP53BP1, were downregulated. Further, the mammary myopithelium marker CK5/6, the mammary hyperplasia marker Ki-67, and other tumor markers were also upregulated. While the exogenous estradiol does not induce the expression of BCL11A, RUNX1, and TP53BP1, the estrogen receptor (ER) agonist Fulvestrant that mimics estradiol action not only elevates estradiol concentrations, but also upregulates tumor marker expression levels, revealing that ER inflammatory inactivation and hyperestrogenemia induction might be the etiological cues of breast cancer origin. This study has preliminarily established a possible correlation of gut microbiota dysbiosis and chronic low-grade inflammation with the early-phase onset of breast cancer in mice. The statistical insignificance of test data was attributed to the individual difference of gut microbiota compositions, which determining the individual and tissue variations of systemic inflammation.


2021 ◽  
Vol 9 (11) ◽  
pp. 2402
Author(s):  
Francesco Di Pierro

Interest in gut microbiota analyses is at an all-time high. Gut microbiota is thought to relate to an increasing range of diseases of interest to physicians and nutritionists. Overweight, obesity, response to diet, metabolic syndrome, low grade inflammation, diabetes and colon neoplasms could maybe be observed in microbiota if affordable markers were available. Possible biomarkers like the Firmicutes/Bacteroidetes ratio, the Gram-positive/Gram-negative ratio, the Prevotella/Bacteroides ratio, and the Fusobacterium nucleatum/Faecalibacterium prausnitzii ratio are here reviewed in a narrative way in the attempt to highlight their possible future role in routine practice and clinically relevant diagnostics.


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