Ontology highlight
ABSTRACT:
PROVIDER: PRJNA721281 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14211333_1.fastq.gz | Fastqsanger.gz | |||
| SRR14211333_2.fastq.gz | Fastqsanger.gz | |||
| SRR14211334_1.fastq.gz | Fastqsanger.gz | |||
| SRR14211334_2.fastq.gz | Fastqsanger.gz | |||
| SRR14211335_1.fastq.gz | Fastqsanger.gz |
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Project description:Physical exercise is a cornerstone for preventing diet-induced obesity, while it is unclear whether physical exercise could offset high-fat, high-calories diet (HFCD)-induced cardiac dysfunction. Here, mice were fed with HFCD and simultaneously subjected to physical exercise. As expected, physical exercise prevented HFCD-induced whole-body fat deposition. However, physical exercise exacerbated HFCD-induced cardiac damage. Further metabolomic analysis results showed that physical exercise induced circulating lipid redistribution, leading to excessive cardiac lipid uptake and lipotoxicity. Our study provides valuable insights into the cardiac effects of exercise in mice fed with HFCD, suggesting that counteracting the negative effect of HFCD by simultaneous physical exercise might be detrimental. Moreover, inappropriate physical exercise may damage certain organs even though it leads to weight loss and overall metabolic benefits. Of note, the current findings are based on animal experiments, the generalizability of these findings beyond this specific diet and mouse strain remains to be further explored.
2024-11-30 | PXD058460 |
Project description:The increasing consumption of high-fat western foods combined with a lack of exercise is a major contributor to the burden of obesity in humans. Aerobic exercise such as running is known to provide metabolic benefits, but how the over-consumption of a high fat diet (HFD) and exercise interact is not well characterized at the molecular level. Here, we examined the plasma proteome in mice for the effects of aerobic exercise as both a treatment and as a preventative regime for animals on either HFD or a healthy control diet. This analysis detected large changes in the plasma proteome induced by the HFD intervention, such as increased abundance of SERPINA7, ALDOB, APOE, and down-regulation of SERPINA1E, CFD (adipsin), LIFR. Some of these changes were only significantly reverted using aerobic exercise as a preventative measure, but not as a treatment regime. To determine if either the intensity, or duration, of exercise influenced the outcome, we compared high-intensity interval training (HIIT) and endurance running. Endurance running slightly outperformed HIIT exercise, but overall both provided similar reversion in abundance of plasma proteins modulated by the high-fat diet including SERPINA7, APOE, SERPINA1E, and CFD. Finally, we compared the changes induced by over-consumption of HFD to previous data from mice fed an isocaloric high saturated fat (SFA) or polyunsaturated fat (PUFA) diet. This identified several common changes including increased APOC2 and APOE, but also highlighted changes specific for either over-consumption of HFD (ALDOB, SERPINA7, CFD), SFA-based diets (SERPINA1E), or PUFA-based diets (Haptoglobin - Hp). Together, these data highlight the importance of early intervention with exercise to revert HFD-induced phenotypes and suggest some of the molecular mechanisms leading to the changes in the plasma proteome generated by high fat diet consumption in both mice and humans.
2020-11-02 | PXD018561 | Pride
Project description:Faecalibacterium prausnitzii, a major commensal bacterium in the human gut, is well known for its anti-inflammatory effects, which improve host intestinal health. Although several studies have reported that inulin, a well-known prebiotic, increases the abundance of F. prausnitzii in the intestine, the mechanism underlying this effect remains unclear. In this study, we applied liquid chromatography tandem mass spectrometry (LC-MS/MS)-based multi-omics approaches to identify biological and enzymatic mechanisms of F. prausnitzii involved in the selective digestion of inulin. An LC-MS/MS-based intracellular proteomic and metabolic profiling was performed to determine the quantitative changes in specific proteins and metabolites of F. prausnitzii when grown on inulin. Interestingly, proteomic analysis revealed that the putative proteins involved in inulin-type fructan utilization by F. prausnitzii, particularly b-fructosidase and amylosucrase were upregulated in the presence of inulin. To investigate the function of these proteins, we overexpressed bfrA and ams, genes encoding beta-fructosidase and amylosucrase, respectively, in Escherichia coli, and observed their ability to degrade fructan. In addition, the enzyme activity assay demonstrated that intracellular fructan hydrolases degrade the inulin-type fructans taken up by fructan ATP-binding cassette transporters. Furthermore, we showed that the fructose uptake activity of F. prausnitzii was enhanced by the fructose phosphotransferase system transporter when inulin was used as a carbon source.
2022-04-04 | PXD030078 | Pride
Project description:Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle. Exercise is known to be beneficial for NAFLD treatment. Recent studies have shown the critical involvement of microRNA in NAFLD. However, it is unclear whether exercise could prevent NAFLD via miRNA targeting. We used microarrays to examine microRNA profiles in high-fat diet fed mice with and without exercise in comparison to normal diet fed mice.
2017-02-09 | GSE65978 | GEO
Project description:Maternal high fat diet may disturb susceptibility in offspring. liver from maternal inulin early intervention has CpG sites that exhibit differential DNA methylationregulated compared to high fat diet.
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Project description:To dentify cecal and liver gene expression changes associated with altered microbiota profiles and reduced weight gain in mice consuming a high-fat diet supplemented with the inulin, or with inulin esterified with propionate and butyrate.
2018-10-01 | GSE106375 | GEO
Project description:Exercise training is a potent treatment of NAFLD and hepatic insulin resistance. Here we provide molecular information about the hepatic mitochondrial metabolism in mice when chronic overnutrition (high-energy diet (HED) for 6 weeks) is combined with exercise training. Training reduced the hepatic triacylglycerol content, fasting insulin, and reversed glucose intolerance. Training modified the hepatic mitochondrial proteome with a decrease in enzymes related to pyruvate metabolism and entry of acetyl-CoA into the TCA cycle. Transcriptome data revealed down-regulation of glucose oxidation and lipogenesis. The mitochondrial respiratory capacity of trained HED-fed mice is increased despite reduced content of complex I. Training decreased diacylglycerol species and JNK phosphorylation, both of which can induce insulin resistance. Increased mitochondrial mass and oxidative capacity of the trained muscle further unburdens the liver from substrate overload. Together, when high fat and carbohydrate intake in mice is accompanied by exercise, the decline of mitochondrial function and insulin resistance can be prevented by modification of mitochondrial acetyl-CoA metabolism.
2022-02-16 | PXD024308 | Pride
Project description:Use untargeted lipidomics to investigate differences in hepatic lipid profile between wild type and knockout mice. Mice were fed with high fat diet for 10 weeks and sacrificed under randomly fed condition. Liver were harvested freshly and frozen into liquid nitrogen immediately. Each sample was combined liver tissues from three individual mice in the same group.
2018-08-02 | MSV000082699 | GNPS
Project description:Background: Non-alcoholic steatohepatitis (NASH) has become one of the most common liver diseases and is still without approved pharmacotherapy. Lifestyle interventions using exercise and diet change remain the current treatment of choice and even a small weight loss (5-7%) can already have a beneficial effect on NASH. However#the underlying molecular mechanisms of exercise and diet interventions remain largely elusive#and it is unclear whether they exert their health effects via similar or different pathways. Methods: Ldlr-/-.Leiden mice received a high fat diet (HFD) for 30 weeks to establish an advanced state of NASH/fibrosis with simultaneous atherosclerosis development. Groups of mice were then either left untreated (control group) or were treated for 20 weeks with exercise (running wheel)#diet change (switch to a low fat chow diet) or the combination thereof. The liver and distant organs including heart#white adipose tissue (WAT) and muscle were histologically examined. Comprehensive transcriptome analysis of liver#WAT and muscle revealed the organ-specific effects of exercise and diet and defined the underlying pathways. Results: Exercise and dietary change significantly reduced body weight#fat mass#adipocyte size and improved myosteatosis and muscle function with additive effects of combination treatment. WAT inflammation was significantly improved by diet change#tended to be reduced with exercise#and combination therapy had no additive effect. Hepatic steatosis and inflammation were almost fully reversed by exercise and diet change#while hepatic fibrosis tended to be improved with exercise and was significantly improved with diet change. Additive effects for the combination therapy were shown for liver steatosis and associated liver lipids#and atherosclerosis#but not for hepatic inflammation and fibrosis. Pathway analysis revealed complementary effects on metabolic pathways and lipid handling processes#thereby substantiating the added value of combined lifestyle treatment. Conclusions: Exercise#diet change and the combination thereof can reverse established NASH/fibrosis in obese Ldlr-/-.Leiden mice. In addition#the lifestyle interventions had beneficial effects on atherosclerosis#WAT inflammation and muscle function. For steatosis and other parameters related to adiposity or lipid metabolism#exercise and dietary change affected more distinct pathways that acted complementary when the interventions were combined resulting in an additive effect for the combination therapy on important endpoints including NASH and atherosclerosis. For inflammation#exercise and diet change shared several underlying pathways resulting in a net similar effect when the interventions were combined.
2021-07-10 | GSE179394 | GEO
Project description:Roseburia inulinivorans is a recently identified motile representative of the Firmicutes that contributes to butyrate formation from a variety of dietary polysaccharide substrates in the human large intestine. Microarray analysis was used here to investigate substrate-driven gene expression changes in R. inulinivorans A2-194. A cluster of fructo-oligosaccharide (FOS)/inulin utilisation genes induced during growth on inulin included one encoding a b-fructofuranosidase protein that was prominent in the proteome of inulin-grown cells. This cluster also included a 6-phosphofructokinase and an ABC transport system, while a distinct inulin-induced 1-phosphofructokinase was linked to a fructose-specific phosphoenolpyruvate-dependent sugar phosphotransferase system (PTS II transport enzyme). Real-time PCR analysis demonstrated that the b-fructofuranosidase and adjacent ABC transport protein showed greatest induction during growth on inulin, whereas the 1-phosphofructokinase enzyme and linked PTS II transport system were most strongly up-regulated during growth on fructose, indicating that these two clusters play distinct roles in the utilization of inulin. The R. inulinivorans B-fructofuranosidase was over-expressed in E. coli and shown to hydrolyse fructans ranging from inulin down to sucrose, with greatest activity on fructo-oligosacharides. Genes induced on starch included the major extra-cellular a-amylase and two distinct a-glucanotransferases together with a gene encoding a flagellin protein. The latter response may be concerned with improving bacterial access to insoluble starch particles.
2010-07-24 | GSE22245 | GEO