Mus musculus
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-32706
PROVIDER: PRJNA147003 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparative transcriptomics and metabolomic analysis of fenofibrate and fish oil treatments in mice
2014-07-03 | E-GEOD-32706 | ExpressionAtlas
Project description:Elevated circulating triglycerides, which are considered a risk factor for cardiovascular disease, can be targeted by treatment with fenofibrate or fish oil. To gain insight into underlying mechanisms, we carried out a comparative transcriptomics and metabolomics analysis of the effect of 2 week treatment withfenofibrate and fish oil in mice. Plasma triglycerides were significantly decreased byfenofibrate (-49.1%) and fish oil (-21.8%), whereas plasma cholesterol was increased by fenofibrate (+29.9%) and decreased by fish oil (-32.8%). Levels of various phospholipid species were specifically decreased by fish oil, while levels of Krebs cycle intermediates were increased specifically by fenofibrate. Plasma levels of many amino acids were altered by fenofibrate and to a lesser extent by fish oil. Both fenofibrate and fish oil upregulated genes involved in fatty acid metabolism, and downregulated genes involved in blood coagulation and fibrinolysis. Significant overlap in gene regulation by fenofibrate and fish oil was observed, reflecting their property as high or low affinity agonist for PPARα, respectively. Fenofibrate specifically downregulated genes involved in complement cascade and inflammatory response. Fish oil specifically downregulated genes involved in cholesterol and fatty acid biosynthesis, and upregulated genes involved in amino acid and arachidonic acid metabolism. Taken together, the data indicate that despite being similarly potent towards modulating plasma free fatty acids, cholesterol and triglyceride levels, fish oil causes modest changes in gene expression likely via activation of multiple mechanistic pathways, whereas fenofibrate causes pronounced gene expression changes via a single pathway, reflecting the key difference between nutritional and pharmacological intervention. Expression profiling of liver from mice fed control diet, fish oil or fenofibrate for 2 weeks.
2011-10-07 | E-GEOD-32706 | biostudies-arrayexpress
Project description:Elevated circulating triglycerides, which are considered a risk factor for cardiovascular disease, can be targeted by treatment with fenofibrate or fish oil. To gain insight into underlying mechanisms, we carried out a comparative transcriptomics and metabolomics analysis of the effect of 2 week treatment withfenofibrate and fish oil in mice. Plasma triglycerides were significantly decreased byfenofibrate (-49.1%) and fish oil (-21.8%), whereas plasma cholesterol was increased by fenofibrate (+29.9%) and decreased by fish oil (-32.8%). Levels of various phospholipid species were specifically decreased by fish oil, while levels of Krebs cycle intermediates were increased specifically by fenofibrate. Plasma levels of many amino acids were altered by fenofibrate and to a lesser extent by fish oil. Both fenofibrate and fish oil upregulated genes involved in fatty acid metabolism, and downregulated genes involved in blood coagulation and fibrinolysis. Significant overlap in gene regulation by fenofibrate and fish oil was observed, reflecting their property as high or low affinity agonist for PPARα, respectively. Fenofibrate specifically downregulated genes involved in complement cascade and inflammatory response. Fish oil specifically downregulated genes involved in cholesterol and fatty acid biosynthesis, and upregulated genes involved in amino acid and arachidonic acid metabolism. Taken together, the data indicate that despite being similarly potent towards modulating plasma free fatty acids, cholesterol and triglyceride levels, fish oil causes modest changes in gene expression likely via activation of multiple mechanistic pathways, whereas fenofibrate causes pronounced gene expression changes via a single pathway, reflecting the key difference between nutritional and pharmacological intervention.
2011-10-08 | GSE32706 | GEO
Project description:The role of PPARα in gene regulation in mouse liver is well characterized. However, less is known about the effect of PPARα activation in human liver. The aim of the present study was to better characterize the impact of PPARα activation on gene regulation in human liver by combining transcriptomics with the use of hepatocyte humanized livers. To that end, chimeric mice containing hepatocyte humanized livers were given an oral dose of 300 mg/kg fenofibrate daily for 4 days. Livers were collected and analysed by hematoxilin and eosin staining, qPCR, and transcriptomics. Transcriptomics data were compared with existing datasets on fenofibrate treatment in normal mice. The human hepatocytes exhibited excessive lipid accumulation. Fenofibrate increased the size of the mouse but not human hepatocytes, and tended to reduce steatosis in the human hepatocytes. Quantitative PCR indicated that induction of PPARα targets by fenofibrate was less pronounced in the human hepatocytes than in the residual mouse hepatocytes. Transcriptomics analysis indicated that, after filtering, a total of 282 genes was significantly different between fenofibrate- and control-treated mice (P<0.01). 123 genes were significantly lower and 159 genes significantly higher in the fenofibrate-treated mice, including many established PPARα targets such as FABP1, HADHB, HADHA, VNN1, PLIN2, ACADVL and HMGCS2. According to gene set enrichment analysis, fenofibrate upregulated interferon/cytokine signaling-related pathways in hepatocyte humanized liver, but downregulated these pathways in normal mouse liver. Also, fenofibrate downregulated pathways related to DNA synthesis in hepatocyte humanized liver but not in normal mouse liver. The results support the major role of PPARα in regulating hepatic lipid metabolism, and underscore the more modest effect of PPARα activation on gene regulation in human liver compared to mouse liver. The data suggest that PPARα may have a suppressive effect on DNA synthesis in human liver, and a stimulatory effect on interferon/cytokine signalling.
2018-05-28 | GSE107041 | GEO
Project description:Atlantic salmon individuals were grown, from fresh water to salt water in tanks on diets with low fish meal (10%) and 1-1.25% total n-3 LC-PUFA levels. Dietary n-3 LC-PUFAs were supplemented by 1) fish oil (FO), 2) Schyzochytrium limacinum biomass (AA). Further, the fish from all treatments were mixed and redistributed in sea cages reared to slaughter (ca. 3kg body weight) on either FO or AA. Transcriptomics analyses in liver and intestinal tissues revealed significant dietary effects on the expression of immune modulating, as well as ion, lipid, protein and xenobiotic metabolism genes.
2019-11-19 | GSE140558 | GEO
Project description:PURPOSE: Previous mouse studies using corn oil (ω-6) as the dietary fat source suggest that decreasing dietary fat content can slow prostate cancer (PCa) growth. However, other studies, in which the diet was composed around saturated fat, showed no difference in outcomes between high-fat and low-fat diets. The relative effects of other fats, such as fish oil and olive oil, also remain unexplored. To our knowledge, no trial has yet compared the effect of various fats on prostate cancer progression. Therefore, we sought to systematically study the effect of fish oil, olive oil, corn oil, and saturated fat on prostate cancer progression. METHODS: A total of 96 male SCID mice were injected with LAPC-4 human PCa cells. Two weeks following injection, mice were singly-housed and randomized to either a fish oil, olive oil, corn oil, or saturated fat based diet. Animals were euthanized when tumors reached 1,000 mm3. Serum was collected at sacrifice and assayed for PSA, insulin, IGF-1, IGFBP-3, and PGE-2 levels. Tumors were also assayed for PGE-2, and COX-2 levels, and gene array analysis was performed. RESULTS: Mice weights and tumor volumes were equivalent across groups at randomization. Overall, fish-oil consumption was associated with improved survival, relative to all other dietary groups (Log-rank, all p<0.05). We did not detect any significant difference in serum PSA, insulin, IGF-1, IGFBP-3, and PGE-2 levels. Glucose at the time of sacrifice was statistically different between groups, with the fish-oil fed mice having the highest levels of serum glucose (Kruskal-Wallis, p=0.03). CONCLUSIONS: In this prostate cancer xenograft model, we found that consuming a diet in which fish-oil was the only fat source slowed tumor growth in improved survival, compared to mice consuming diets composed of olive oil, corn oil, or saturated fat sources. These results suggest that type of dietary fat consumed may be as important as amount of dietary fat consumed in the setting of prostate cancer.
2016-01-01 | GSE40654 | GEO
Project description:Dietary effects of arachidonate-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression.<BR> <LI><u>Brain:</u></LI><BR> GSM2558: Control<bR> GSM2559: Control <bR> GSM2560: Fungal oil (AA)<bR> GSM2561: Fungal oil (AA)<bR> GSM2562: Fish oil (DHA)<bR> GSM2563: Fish oil (DHA)<bR> GSM2564: Fish and Fungal oil (DHA + AA)<bR> <LI><u>Liver:</u></LI><bR> GSM2565: Control <bR> GSM2566: Control<bR> GSM2567: Control<bR> GSM2568: Control<bR> GSM2569: Fungal oil (AA)<bR> GSM2570: Fungal oil (AA)<bR> GSM2571: Fish oil (DHA)<bR> GSM2572: Fish oil (DHA)<bR> GSM2573: Fish + Fungal oil (DHA +AA)<bR> GSM2574: Fish + Fungal oil (DHA +AA)<bR> Keywords: ordered
2002-11-11 | GSE91 | GEO
Project description:We used microarray analysis to examine which genes are differentially expressed in mice that received a combination of fish oil and indomethacin.
2012-11-06 | GSE23742 | GEO
Project description:We used microarray analysis to examine which genes are differentially expressed in mice that received a combination of fish oil and indomethacin. We fed low density lipoprotein receptor knock-out (LDLR-/-) mice with 6% of olive oil (control) or fish oil diets in the presence or absence of indomethacin for 12 weeks. We collected total RNA from liver samples and pooled 6 RNA samples in each group for Affymetrix microarrays.
2012-11-06 | E-GEOD-23742 | biostudies-arrayexpress
Project description:The marine bacterium Rhodococcus erythropolis PR4 was demonstrated to be able for assimilation/biodegradation of hydrocarbons. Not just the chromosome but two large plasmids provide versatile enzyme sets involved in many metabolic pathways. In order to identify the key elements involved in biodegradation of the model compound, hexadecane, and diesel oil, we performed whole transcriptome analysis on cells grown in the presence of n-hexadecane and diesel oil. Sodium acetate grown cells were used as control. The final goal of the project is a comparative transcriptomic analysis of Rhodococcus erythropolis PR4 cells grown on acetate, on the model compound: hexadecane and the real substrate: diesel oil. Comparative transcriptomics of Rhodococcus erythropolis PR4 grown on n-hexadecane, diesel oil, and sodium acetate.
2014-04-21 | E-GEOD-56474 | biostudies-arrayexpress