Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA137145 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We have demonstrated that fish oil/pectin (FO/P) diets protect against colon cancer compared to corn oil/cellulose (CO/C) by upregulating apoptosis and suppressing proliferation. To elucidate the mechanisms whereby FO/P diets induce apoptosis and suppress proliferation during the tumorigenic process, we analyzed the temporal gene expression profiles from exfoliated rat colonocytes. KEYWORDS: Fish oil/pectin, pectin, exfoliated colonocytes, gene expression, apoptosis, colon cancer, chemoprevention
2012-02-20 | GSE27266 | GEO
Project description:We have demonstrated that fish oil/pectin (FO/P) diets protect against colon cancer compared to corn oil/cellulose (CO/C) by upregulating apoptosis and suppressing proliferation. To elucidate the mechanisms whereby FO/P diets induce apoptosis and suppress proliferation during the tumorigenic process, we analyzed the temporal gene expression profiles from exfoliated rat colonocytes. KEYWORDS: Fish oil/pectin, pectin, exfoliated colonocytes, gene expression, apoptosis, colon cancer, chemoprevention Rats consumed diets containing FO/P or CO/C and were injected with azoxymethane (AOM, 2x, 15 mg/kg BW, s.c.). Feces collected at the initiation, aberrant crypt foci (ACF), and tumor stages of colon cancer (24 h (n=20), 7 wk (n=37), and 28 wk (n=28) after AOM injection, respectively) was used for poly A(+) RNA extraction. Gene expression signatures were determined using Codelink arrays.
2012-02-20 | E-GEOD-27266 | biostudies-arrayexpress
Project description:In an effort to gain insight into the extensive dimension of post-translational modifications in histones (including H3K4me3 and H3K9ac) and elucidate the chemoprotective impact of dietary bioactive compounds on transcriptional control in a colon cancer preclinical model, we generated high-resolution genome-wide RNA (RNA-Seq) and “chromatin-state” (H3K4me3-seq and H3K9ac-seq) maps for intestinal (epithelial colonocytes) crypts in rats treated with a colon carcinogen and fed bioactive (i) fish oil (ii) butyrate (in the form of a fermentable fiber a rich source of SCFA), (iii) a combination of fish oil plus butyrate or (iv) control diets. Poor correlation was observed between differentially transcribed (DE) and enriched genes (DERs) at multiple epigenetic levels in fat x fiber dietary combinations and in the presence/absence of carcinogen. We also demonstrated that the combinatorial diet (fish oil + pectin) was synergistically chemoprotective, and uniquely affected epigenetic profiles in the intestinal epithelium, e.g., upregulating lipid catabolism and beta-oxidation associated genes.
2017-09-08 | GSE87525 | 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:Dietary effects of arachidonate-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression.; Brain:; GSM2558: Control; GSM2559: Control ; GSM2560: Fungal oil (AA); GSM2561: Fungal oil (AA); GSM2562: Fish oil (DHA); GSM2563: Fish oil (DHA); GSM2564: Fish and Fungal oil (DHA + AA); Liver:; GSM2565: Control ; GSM2566: Control; GSM2567: Control; GSM2568: Control; GSM2569: Fungal oil (AA); GSM2570: Fungal oil (AA); GSM2571: Fish oil (DHA); GSM2572: Fish oil (DHA); GSM2573: Fish + Fungal oil (DHA +AA); GSM2574: Fish + Fungal oil (DHA +AA)
2007-12-13 | E-GEOD-91 | 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:Novel DHA-enriched oils with high α-linolenic acid (ALA) content will be available in the near future as an alternative for dietary fish oil replacement in aquafeeds. As preliminary validation, we 1) assessed the ability of a diet containing a formulated oil blend (tuna oil + flaxseed oil, TOFX) with high DHA and ALA content to achieve fish oil-like omega-3 long-chain (≥C20) polyunsaturated fatty acids (n-3 LC-PUFA) tissue composition in Atlantic salmon smolts, and 2) applied liver proteomics as exploratory approach to understand the consequent nutritional changes. Comparisons were made on fish fed a fish oil-based diet (FO) and a commercial-like oil blend diet (fish oil + poultry oil, FOPO) over 89 days. Growth and feed efficiency ratio were lower on the TOFX diet. Fish tissue concentration of n-3 LC-PUFA and the n-3:n-6 ratio were significantly higher for TOFX than for FOPO, but not higher than for FO, while tissue retention efficiency of n-3 LC-PUFA was promoted by TOFX relative to FO. Proteomics analysis revealed an unexpected oxidative stress response as the main adaptive physiological mechanism in TOFX fish. While specific dietary fatty acid concentrations and balances and antioxidant supplementation may need further attention, the use of an oil with a high content of DHA and ALA can enhance tissue deposition of n-3 LC-PUFA in relation to a commercially used blend oil.
2018-03-01 | PXD004114 | Pride
Project description:Fish oil, olive oil, and coconut oil dietary supplementation have several cardioprotective benefits, but it is not established if they can protect against air pollution-induced adverse effects. We hypothesized that these dietary supplements would attenuate ozone-induced systemic and pulmonary effects. Male Wistar Kyoto rats were fed either a normal diet, or a diet enriched with fish, olive, or coconut oil starting at 4 weeks of age for 8 weeks. Animals were then exposed to air or ozone (0.8 ppm), 4h/day for 2 consecutive days. The fish oil diet completely abolished phenylephrine-induced vasoconstriction that was increased following ozone exposure in the animals fed all other diets. Only the fish oil diet increased baseline levels of bronchoalveolar lavage fluid (BALF) markers of lung injury and inflammation. Ozone-induced pulmonary injury/inflammation were comparable in rats on normal, coconut oil, and olive oil diets with altered expression of markers in animals fed the fish oil diet. Fish oil, regardless of exposure, led to enlarged, foamy macrophages in the BALF that coincided with decreased mRNA expression of cholesterol transporters, cholesterol receptors, and nuclear receptors in the lung. Serum miRNA profile was assessed using small RNA-sequencing in normal and fish oil groups and demonstrated marked depletion of a variety of miRNAs, several of which were of splenic origin. No ozone-specific changes were noted. Collectively, these data indicate that while fish oil offered protection from ozone-induced aortic vasoconstriction, it increased pulmonary injury/inflammation and impaired lipid transport mechanisms resulting in foamy macrophage accumulation, demonstrating the need to be cognizant of potential off-target pulmonary effects that might offset the overall benefit of this vasoprotective dietary supplement.
2018-01-11 | GSE102015 | GEO
Project description:Fish oil supplementation has been shown to alter gene expression of mononuclear cells both in vitro and in vivo. However, little is known about the total transcriptomic profile in healthy subjects after intake of fish oil compared to a control group. The objective was to examine the gene expression profile in peripheral blood mononuclear cells (PBMCs) in healthy subjects after intake of fish oil for seven weeks using whole-genome transcriptomic analysis. In a double-blinded randomized controlled study, healthy subjects received capsules containing either 8 g/d of fish oil (1.6 g/d EPA+DHA) (n=17) or 8 g/d of high oleic sunflower oil (n=19) for seven weeks. The results provide important information on how fish oil may modulate basic cellular processes involved in normal cell function and lymphocyte activation such as ER stress, cell cycle and apoptosis.
2014-05-01 | GSE48368 | 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