Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA137145 | ENA |
REPOSITORIES: ENA
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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:To assess the utility of diet modulation as a promising avenue to modulate ferroptosis in the colon, we examined the combinatorial effect of n-3 vs. n-6 polyunsaturated fatty acids (PUFA) and highly fermentable vs. poorly fermentable fiber on ferroptosis induction in preclinical models and healthy human adults. In vitro treatment of immortalized mouse colonocytes with docosahexaenoic acid, a n-3 PUFA enriched in fish oil, and butyrate, a short chain fatty acid generated by colonic microbial fermentation of fiber, reduced cell viability and interactively (P < 0.05) increased lipid peroxidation, a key biomarker for ferroptosis, compared to counterpart treatments. Addition of the ferroptosis inhibitor, ferrostatin-1, significantly blocked the combined effects of docosahexaenoic acid and butyrate on colonocyte lipid oxidation and cell death in vitro. In vivo treatment of mice fed fish oil and highly fermentable fiber (pectin) vs. control, corn oil (contains n-6 PUFA) and poorly fermentable fiber (cellulose) significantly (P < 0.05) promoted lipid peroxidation and the induction of ferroptosis transcriptional networks exclusively in colonic epithelial cells. In addition, as part of a randomized controlled crossover pilot study in humans, supplemental fermentable fiber (35 g/d soluble corn fiber) and fish oil (6 g/d n-3 PUFA) upregulated intestinal ferroptosis related gene expression, as compared to similar doses of maltodextrin plus corn oil. Our findings demonstrate that dietary fish oil and fermentable fiber act synergistically to induce ferroptosis in colonocytes. These important and often overlooked interactions between diet and the gut microbiome help to explain the anti-cancer benefit of the pesco-vegetarian diet.
2026-03-18 | GSE295395 | GEO
Project description:To assess the utility of diet modulation as a promising avenue to modulate ferroptosis in the colon, we examined the combinatorial effect of n-3 vs. n-6 polyunsaturated fatty acids (PUFA) and highly fermentable vs. poorly fermentable fiber on ferroptosis induction in preclinical models and healthy human adults. In vitro treatment of immortalized mouse colonocytes with docosahexaenoic acid, a n-3 PUFA enriched in fish oil, and butyrate, a short chain fatty acid generated by colonic microbial fermentation of fiber, reduced cell viability and interactively (P < 0.05) increased lipid peroxidation, a key biomarker for ferroptosis, compared to counterpart treatments. Addition of the ferroptosis inhibitor, ferrostatin-1, significantly blocked the combined effects of docosahexaenoic acid and butyrate on colonocyte lipid oxidation and cell death in vitro. In vivo treatment of mice fed fish oil and highly fermentable fiber (pectin) vs. control, corn oil (contains n-6 PUFA) and poorly fermentable fiber (cellulose) significantly (P < 0.05) promoted lipid peroxidation and the induction of ferroptosis transcriptional networks exclusively in colonic epithelial cells. In addition, as part of a randomized controlled crossover pilot study in humans, supplemental fermentable fiber (35 g/d soluble corn fiber) and fish oil (6 g/d n-3 PUFA) upregulated intestinal ferroptosis related gene expression, as compared to similar doses of maltodextrin plus corn oil. Our findings demonstrate that dietary fish oil and fermentable fiber act synergistically to induce ferroptosis in colonocytes. These important and often overlooked interactions between diet and the gut microbiome help to explain the anti-cancer benefit of the pesco-vegetarian diet.
2026-03-18 | GSE295394 | GEO
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: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: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: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