Project description:Folic acid deficiency is common worldwide and is linked to intestinal flora imbalance. The intestinal microbial utilization of folic acid based on model animals faces the challenges of repeatability and individual variability. In this study, we built an in vitro fecal slurry culture model deficient in folic acid. We examined the effects of supplementation with different forms of folic acid (5-methyltetrahydrofolate and non-reduced folic acid) on the modulation of intestinal flora. 16S rDNA gene sequencing showed alpha diversity increased after folic acid supplementation compared to fermentation samples with folic acid deficiency. In the non-reduced folic acid (FA) group, the relative abundance of the Firmicutes phylum dropped to 56.7%, whereas in the 5-methyltetrahydrofolate (MTHF) supplementation group, it grew to 64.9%. Lactobacillus genera became more prevalent, reaching 22.8% and 30.8%, respectively. Additionally, Bifidobacterium and Pedioccus, two common probiotic bacteria, were in higher abundance. Short-chain fatty acids (SCFAs) analysis showed that supplementation with folic acid (non-reduced folic acid, 5-methyltetrahydrofolate) decreased acetic acid and increased the fermentation yield of isobutyric acid. The in vitro fecal slurry culture model developed in this study can be utilized as a human folic acid deficiency model for studying intestinal microbiota and demonstrated that both 5-methyltetrahydrofolate and non-reduced folic acid have effects on the regulation of intestinal microecology.
Project description:Herein, we evaluated the regulation of plantaricin NC8 on gut microbiota by in vitro simulation system, and assessed their modulation on different intestinal types, namely enterotype 1 (ET B) and enterotype 2 (ET P), for the first time. Plantaricin NC8 could not significantly promote or inhibit the production short chain fatty acids (SCFAs) by the gut flora in the fecal samples from eight subjects to produce through Gas chromatography (GC) determining, neither ET B nor ET P. 16S rDNA sequencing showed that plantaricin NC8 shortened the Shannon index of ET B and the Simpson index of ET P, but their β diversity change was not statistically significant. In addition, plantaricin NC8 could promote the growth of beneficial bacteria. Results showed that plantaricin NC8 mainly increased the abundance of Actinobacterias, Bacteroides, Bifidobacterium, Megamonas, Escherichia-Shigella, and decreased the abundance of Streptococcus in ET B. And it also increased the abundance of Prevotella_9, Bifidobacterium, Escherichia-Shigella, Mitsuokella and others in ET P. Plantaricin NC8 can influence intestinal microorganisms, but the influence were different for different enterotypes.
Project description:<p>There is increased appreciation for the roles of the gut-liver axis in liver and gall diseases. Specific gut microbes are associated with susceptibility to gallstone diseases,while the relationship between intestinal flora and liver metabolism in the formation of gallstones remains unclear. C57BL/6J male mice received a dietary intervention for 8 weeks, with a lithogenic diet given to the test group and a normal diet to the control group. An integrated 16S rRNA gene sequencing and LC/MS-based nontargeted metabolomics approach was performed to explore the impact of the lithogenic diet on the intestinal flora and liver metabolic phenotype, and Spearman correlation analysis established a network between the gut and liver. </p>
Project description:Intestinal flora is a key factor in insulin resistance and contribute to the development of polycystic ovary syndrome and ameliorates glucose metabolism via activation of intestinal farnesoid X receptor (Mice)
Project description:There are 10 mice in the experiment, named REC. The mice were fed with high salt diets (5% NaCl) for 4 weeks and then fed with normal salt diets for 4 weeks. Then extracted DNA from mice gastric flora to detect changes in the gastric flora of mice.
Project description:Intestinal flora is a key factor in insulin resistance and contribute to the development of polycystic ovary syndrome and ameliorates glucose metabolism via activation of intestinal farnesoid X receptor (Human)