Ontology highlight
ABSTRACT:
PROVIDER: PRJNA480760 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7513230.fastq.gz | Fastqsanger.gz | |||
| SRR7513240.fastq.gz | Fastqsanger.gz | |||
| SRR7513250.fastq.gz | Fastqsanger.gz | |||
| SRR7513260.fastq.gz | Fastqsanger.gz | |||
| SRR7513270.fastq.gz | Fastqsanger.gz |
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Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.
2023-10-03 | GSE232128 | GEO
Project description:The attenuating effects of green tea supplements (GTS) against the ultraviolet (UV) radiation induced skin damages are distinguished. However, the concomitant effects of GTS on the large intestinal microbiomes and associated metabolomes are largely unclear. Herein, we performed an integrated microbiome-metabolome analysis to uncover the esoteric links between gut microbiome and exo/endogenous metabolome maneuvered in the large intestine of UVB-exposed mice subjected to dietary GTS. In UVB-exposed mice groups (UVB), class Bacilli and order Bifidobacteriales were observed as discriminant taxa with decreased lysophospholipid levels compared to the unexposed mice groups subjected to normal diet (NOR). Conversely, in GTS fed UVB-exposed mice (U+GTS), the gut-microbiome diversity was greatly enhanced with enrichment in the classes, Clostridia and Erysipelotrichia, as well as genera, Allobaculum and Lachnoclostridium. Additionally, the gut endogenous metabolomes changed with an increase in amino acids, fatty acids, lipids, and bile acids contents coupled with a decrease in nucleobases and carbohydrate levels. The altered metabolomes exhibited high correlations with GTS enriched intestinal microflora. Intriguingly, the various conjugates of green tea catechins viz., sulfated, glucuronided, and methylated ones including their exogenous derivatives were detected from large intestinal contents and liver samples. Hence, we conjecture that the metabolic conversions for the molecular components in GTS strongly influenced the gut micro-environment in UVB-exposed mice groups, ergo modulate their gut-microbiome as well as exo/endogenous metabolomes.
2018-09-14 | MTBLS527 | MetaboLights
Project description:The effects of increasing addition of green tea in dietary changes the bacterial populations in broiler ileum were evaluated. Four hundreds of AA broilers were randomly assigned to four groups with green tea addition of 0, 0.5, 1 and 2 percent in the diet. The body weight showed no difference but a digital increase positively correlated with addition of green tea. The content of green tea had a linear effect of lengthening the ileum villi. The barcoded DNA pyrosequencing method was used to reveal 15 phyla, 1157phylotypes and 3098 16S operational taxonomic units (OTUs). The most predominant bacterial phyla were Firmicutes (56.89%), Actinobacteria (30.58%), Proteobacteria (8.61%) and Bacteroidetes (2.72%). As the proportion of additional green tea increased, the abundance of phylum Actinobacteria (p=0.003) and Proteobacteria (p=0.049) almost linearly increased, while the proportion of Firmicutes (p=0.027) linearly decreased. Only 2 OTUs were significantly affected by the increased additive, Corynebacteriaceae (p=0.011) and Staphylococcaceae (p= 0.006). Triplot analysis suggested that the dominant phyla of Verrucomicrobia, TM7 and Actinobacteria were clearly related to the addition of green tea. Moreover, green tea addition influenced the construction of microbiota, and lengthened the villus in ileum by Monte Carlo permutation test. These findings provide a new understanding of the ileal microbial ecology, which may be useful in modulating the gut microbiome, and also the proper usage of powdered green tea.
2015-09-29 | GSE73516 | GEO
Project description:Constant availability of food can contribute to the pathogenesis of metabolic syndrome and type 2 diabetes. Short term intermittent fasting (IF) can reset the central, light-entrained (suprachiastmatic nucleus) clock and also the peripheral, food-entrained (liver) clock to restore metabolic homeostasis in T2D. We asked if long term IF could prevent development of diabetic retinopathy (DR) in a type 2 diabetes model, the db/db mouse. After 7 months, IF corrected diabetes-induced increases in triglycerides, cholesteryl esters and diglycerides. IF protocol in db/db mice also prevented development of DR. In addition, host frequency and time of food intake affected the gut microbiome composition. IF led to decreased levels of Clostridiales and Akkermansia muciniphila in db/db mice and these changes in flora were accompanied by increased gut mucin, goblet cell number and villus length. Increased levels of Firmicutes in db/db mice on IF supported improved bile acid metabolism. To confirm that the restoration of bile acid function could contribute to the beneficial effects induced by IF on DR, the dual FXR/TGR-5 agonist INT-767 was administered to a second diabetes model, DBA2J mice injected with streptozotocin (STZ) and placed on Western diet (WD). In this model, INT-767 prevented development of DR. These findings support the concept that long-term IF mediates multiple beneficial effect by restoring the gut-liver axis homeostasis.
2018-12-31 | GSE100230 | GEO
Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice.
2012-03-29 | GSE36875 | GEO
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice. Mice were divided into three groups: Non-diabetic controls (db/+), untreated diabetic controls (db-c), and rosiglitazone-treated diabetic mice (db-t). Whole-heart RNA from five mice from each of the three groups after four months with or without treatment was used for microarray analysis.Universal Reference RNAs for mouse (Stratagene, La Jolla, CA) were purchased as microarray reference controls.
2012-03-28 | E-GEOD-36875 | biostudies-arrayexpress