The influence of long-term use of diet enriched with biologically active substances on transcirptomic profile in rats liver
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Hanna Oszkiel
PROVIDER: E-GEOD-51657 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The aim of this study was to evaluate the ability of a diet enriched with biologically active compounds to protect against 1,2-dimethylhydrazine - induced carcinogenesis in 14-month old rats liver. Rats from control and experimental groups after 14 months of experiment were given 5 times 1,2-dimethylhydrazine (DMH) by intraperitoneal treatment at a dose of 30mg/kg of body weight once a week to induce the process of carcinogenesis. RNA from their livers were hybridized to Agilent two color microarrays with a common reference. Then, the transcriptomic profile of these livers were compared to the transcriptomic profile of 14-month rats received the same control diet and diet enriched with biologically active substances, but without 1,2-dimethylhydrazine - induction (data from GEO Submission - GSE51657).
2014-02-27 | E-GEOD-55378 | biostudies-arrayexpress
Project description:During the last few decades, the long-lasting consequences of nutritional programming during the early phase of life have become increasingly evident, but the effects of maternal nutrition on the developing intestine are currently still relatively underexplored. In this study, we investigated in mice the effects of a maternal Western-style (WS) high fat/cholesterol diet, given during the perinatal period, on gene expression and microbiota composition of two-week-old offspring. Microarray analysis revealed that a perinatal WS diet caused significant changes in gene expression in the small intestine and colon of the suckling offspring. A strong sexually dimorphic effect was observed in the affected genes. However, pathway analysis of the differentially expressed genes displayed that in both sexes metabolic and immune functions were strongly affected. Integration of the microbiota and gene expression data applying a multivariate correlation analyses revealed that Bacteroidaceae, Porphyromonadaceae and Lachnospiraceae were the bacterial families that most strongly correlated with gene expression in the colon and not with the bacterial families displaying the most pronounced change due to perinatal exposure to a WS diet. Amongst the genes demonstrating a strong correlation with one or more bacterial families were genes of key importance for intestinal development or functioning (i.e., Pitx2 and Ace2). In conclusion, our data demonstrate a strong programming effect of a maternal WS diet on the development of the intestine in the offspring. Small intestine and colon were isolated from two-week-old pups of dams fed a low- or Western-style high fat/cholesterol diet and subjected to gene expression profiling.
2016-08-22 | E-GEOD-72705 | biostudies-arrayexpress
Project description:Since the liver is the central organ of metabolism, changes in diet have a great impact on this organ and overall on health with aging. It is well known that dietary fat source strongly influences many parameters of the hepatic mitochondria. These changes includes modification of lipid composition of mitochondrial membrane, affecting the mtETC functions, oxidative stress and mtDNA alterations. We used microarrays to detail the changes in gene expression provides by feeding lifelong on different dietary fat sources, and identified distinct classes of up and down-regulated genes during aging under different dietary conditions. Rats were fed lifelong on a normolipidic diet (4% w/w) with virgin olive, sunflower or fish oil as dietary fat source. At 6 and 24 months, animals were killed and liver were removed for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain changes in gene expression due to both aging and dietary conditions. There were 6 experimental groups (virgin olive oil at 6 months, sunflower oil at 6 months, fish oil at 6 months, virgin olive oil at 24 months, sunflower oil at 24 months and fish oil at 24 months. 3 animals were studied of each experimental group, so a total of 18 samples were analyzed.
2014-03-26 | E-GEOD-56166 | biostudies-arrayexpress
Project description:Maternal diet is associated with the development of metabolism-related and other non-communicable diseases in offspring. Underlying mechanisms, functional profiles, and molecular markers are only starting to be revealed. Here, we explored the physiological and molecular impact of maternal Western-style diet on the liver of male and female offspring. C57BL/6 dams were exposed to either a low fat/low cholesterol diet (LFD) or a Western-style high fat/high cholesterol diet (WSD) for six weeks before mating, as well as during gestation and lactation. Dams and offspring were sacrificed at postnatal day 14, and body, liver, and blood parameters were assessed. The impact of maternal WSD on the pups' liver gene expression was characterised by whole-transcriptome microarray analysis. Exclusively male offspring had significantly higher body weight upon maternal WSD. In offspring of both sexes of WSD dams, liver and blood parameters, as well as hepatic gene expression profiles were changed. In total, 686 and 604 genes were differentially expressed in liver (pM-bM-^IM-$0.01) of males and females, respectively. Only 10% of these significantly changed genes overlapped in both sexes. In males, in particular alterations of gene expression with respect to developmental functions and processes were observed, such as Wnt/beta-catenin signalling. In females, mainly genes important for lipid metabolism, including cholesterol synthesis, were changed. We conclude that maternal WSD affects physiological parameters and induces substantial changes in the molecular profile of the liver in two-week-old pups. Remarkably, the observed biological responses of the offspring reveal pronounced sex-specificity. C57BL/6 dams were exposed to either a low fat/low cholesterol diet (LFD) or a Western-style high fat/high cholesterol diet (WSD) as six weeks pre-treatment before mating, as well as during gestation and lactation. Offspring were sacrificed at postnatal week two, livers were removed and RNA samples were subjected to gene expression profiling.
2013-11-27 | E-GEOD-46359 | biostudies-arrayexpress
Project description:Background. Resistant Starch (RS) improves CKD outcomes. In this report we study how RS modulates host-microbiome interactions in CKD by measuring changes in abundance of proteins and bacteria in the gut. In addition, we demonstrate RS-mediated reduction in CKD-induced kidney damage. Methods. Eight mice underwent 5/6 nephrectomy to induce CKD and 8 served as healthy controls. CKD and Healthy (H) groups were further split into those receiving RS (CKDRS, n=4; HRS, n=4) and those on normal diet (CKD, n=4, H, n=4). Kidney injury was evaluated by measuring BUN/creatinine and by most-mortem histopathological evaluation. Cecal contents were analyzed mass spectrometry-based metaproteomics. PEAKS Studio was used to identify peptides via de novo sequencing. A set of R/Bioconductor packages and in house written scripts was further used to infer bacteria present, to evaluate changes in proteins and bacterial abundances, and to perform statistical analysis and hierarchical clustering. Results. The 5/6 nephrectomy compromised kidney function as seen by an increase in creatinine and BUN. Representative photomicrographs of trichrome-stained kidney sections showed reduced tubulointerstitial injury in CKD mice fed HAM-RS2 diet comparing to CKD mice fed normal diet. Identified organisms and proteins point toward a higher population of butyrate-producing bacteria, and reduced abundance of mucin-degrading bacteria. Conclusion. Resistant starch slows the progression of chronic kidney disease. Gut barrier function through maintenance of the mucin barrier plays a role in RS-associated improvements in CKD phenotype. Resistant starch supplementation leads to the active bacterial proliferation and the reduction of harmful bacterial metabolites.
2020-10-19 | PXD019623 | Pride
Project description:Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls fed methyl donor sufficient diets
2012-04-30 | E-GEOD-37010 | biostudies-arrayexpress
Project description:The aim of the study was to identify genes which are differentially expressed in the liver from rat fed with control diet and rat fed with diet enriched with biologicaly active compounds after 3 and 14 months of experiment
2013-10-25 | GSE51657 | GEO
Project description:Background: Previously, we reported that perfluorooctanoic acid (PFOA) promotes liver cancer in manner similar to that of 17β-estradiol (E2) in rainbow trout. Also, other perfluoroalkyl acids (PFAAs) are weakly estrogenic in trout and bind the trout liver estrogen receptor (ER). Objectives: The primary objective of this study was to determine whether multiple PFAAs enhance hepatic tumorigenesis in trout, an animal model that represents human insensitivity to peroxisome proliferators. Methods: A two-stage chemical carcinogenesis model was employed in trout to evaluate PFOA, perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorooctane sulfonate (PFOS) and 8:2 fluorotelomer alcohol (8:2FtOH) as complete carcinogens or promoters of aflatoxin B1 (AFB1)- and/or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced liver cancer. A custom trout DNA microarray was used to assess hepatic transcriptional response to these dietary treatments in comparison to E2 and the classic peroxisome proliferator clofibrate (CLOF). Results: Incidence, multiplicity and size of liver tumors in trout fed diets containing E2, PFOA, PFNA and PFDA were significantly higher compared to AFB1-initiated animals fed control diet, whereas PFOS caused a minor increase in liver tumor incidence. E2 and PFOA also enhanced MNNG-initiated hepatocarcinogenesis. Pearson correlation analyses, unsupervised hierarchical clustering and principal components analyses showed that the hepatic gene expression profiles for E2 and PFOA, PFNA, PFDA and PFOS were overall highly similar, though distinct patterns of gene expression were evident for each treatment, particularly for PFNA. Conclusions: Overall, these data suggest that multiple PFAAs can promote liver cancer and that the mechanism of promotion may be similar to that for E2. A total of 40 samples were analyzed using a a dye-swap, reference sample hybridization protocol. Rainbow trout were exposed to the following experimental treatments via the diet for two weeks (number in parenthesis is assigned group #): (1) Control; (2) 5 mg/kg diet estradiol (E2); (3) 2000 mg/kg diet perfluorooctanoic acid (PFOA); (4) 2000 mg/kg diet perfluorononanoic acid (PFNA); (5) 2000 mg/kg diet perfluorodecanoic acid (PFDA); (6) 200 mg/kg diet perfluorooctane sulfonate; (7) 2000 mg/kg 8:2 fluorotelomer alcohol (FTOH); and (8) 2000 mg/kg diet clofibrate. A total of 40 total hepatic mRNA samples were analyzed using a dye-swap, reference sample hybridization protocol. A reference RNA pool was made by combining equal amounts of RNA from all control RNA samples, with one exception. A separate time-matched reference pool was utilized for group 6 samples (PFOS treatment). Five hybridizations were performed for each treatment group in the following pattern: Replicate A Cy5/Reference Cy3; Replicate A Cy3/Reference Cy 5; Replicate B Cy5/Reference Cy3; Replicate B Cy3/Reference Cy5; Replicate C Cy5/Reference Cy3. Thus, the experiment consisted of three biological replicates, for two of which were replicated technically.
2011-08-01 | E-GEOD-31085 | biostudies-arrayexpress
Project description:Weanling rats fed a choline-deficient diet develop acute renal failure (ARF) after 6-7 days of receiving the experimental diet. Its pathogenesis is controversial. Menhaden oil has a protective effect in this experimental model. The aim of this study is to describe both the genetic profile and its changes when vegetable oils are replaced by menhaden oil. Wistar, weanling rats from the Animal Facility of the Centre of Experimental and Applied Pathology were divided into 4 groups and fed with the following diets: 1- Choline-deficient diet with vegetable oils as lipids (corn and hydrogenated oils); 2- Choline-supplemented diet with vegetable oils as lipids; 3- Choline-deficient diet with menhaden oil as lipid; and 4- Choline supplemented diet with menhaden oil as lipid. Animals were sacrificed after 6 days of receiving the experimental diets. The right kidney was cryopreserved. In this assay biological duplicated samples were used. In order to evaluate changes in gene expression WT Expression Kit (Ambion, USA) over the platform GeneChip® Gene 1.0 ST Rat Genome Array (Affymetrix Inc, USA) was used. Fluorescent distribution in the array was obtained using the language R (www-r-project.org), in house own algorithms and other formsbioconductor tools http://www.bioconductor.org/. We analyzed the differential gene expression, using as cut value p<0.01 with fdr control & |log FC|>1.5, in all groups. Rats fed with diets 2, 3 and 4 have similar genetic profiles. However, the comparison between rats fed with diets 2 and 4 showed 35 genes with diferential expression. As these rats did not have renal necrosis, we can hypothesize that the differential expression is due to the menhaden oil of the diet. In short, the massive analysis of genetic expression allowed to confirm that menhaden oil has a protective effect in this experimental model and to identify 35 genes that could be responsible of that protection. Twenty eight animals were sacrificed after 6 days of receiving the experimental diets. The right kidney was cryopreserved for microarray analysis. Cryopreserved kidney was pulverized under liquid-nitrogen conditions. Total RNA was purified from 30 mg of frozen rat kidney tissue. Each sample represents a pool of 3 animals (except CD+AM SN with 2 animals/pool), to reduce biological variation. In this assay biological duplicated samples were used.
2011-12-06 | E-GEOD-34139 | biostudies-arrayexpress
Project description:The aim of this study was to evaluate whether the dietary treatment with olive oil phenols modifies the profile of microRNA and gene expression in different areas of the aging mouse brain and to correlate these changes with the cognitive and motor changes observed in the same aging animals. C57Bl/6J mice were fed from middle age to senescence with extra-virgin olive oil (10% wt/wt dry diet) rich in polyphenols (H-EVOO group, total polyphenol dose/day, 6mg/kg) or with the same extra-virgin olive oil deprived of phenolic compounds (L-EVOO group). By whole gene expression analysis we identified 53 genes differentially expressed in the cortex of H-EVOO mice compared to L-EVOO mice and no genes differentially expressed in the cerebellum. Gene Set Expression analysis (GSEA) found 6 gene sets significantly modulated by the dietary treatments in cortex, like the agrin-related postsynaptic differentiation gene set, involved in cholinergic synaptic differentiation and maintenance, exerting effects on axonal and dendritic growth. miRNA profiling found only 6 miRNA differentially modulated after 12 months of feeding and 63 after six months. Among them we noted miRNAs previously associated to neurodegenerative disorders such as mir101, 8.5 time more expressed in the cortex of L-EVOO fed mice compared to the H-EVOO group and no expressed in young mice. We extended our analysis on cortex harvested from transgenic TgCRND8 mice, a model of Alzheimer's disease, observing an overall down-regulation of miRNAs compared to mice of the same age. On the contrary, the H-EVOO fed mice cortex showed expression profiles similar to those of young mice, results supporting our previous data demonstrating that extra virgin olive oil rich in polyphenols may improve some age-related dysfunctions.
2013-09-10 | E-MTAB-1530 | biostudies-arrayexpress