Microarray examination of liver tissue from mice fed 58% saturated high fat diet to induce hepatic steatosis.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Marcus Lyall
PROVIDER: E-MTAB-5520 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Background: Post-menopausal obesity is an established risk factor for breast cancer. Consumption of diets high in fat is known to be highly correlated with obesity. In this, we sought to evaluate the interaction(s) between high fat diet, weight gain and mammary carcinogenesis using an obese-resistant and obese-prone rat model with direct correlates to human disease. Methods: Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly. Results: The DMBA-treated OR rats on the 39% safflower diet had significantly greater incidence of ductal carcinoma-in-situ (DCIS) lesions and significantly greater DCIS multiplicity than DMBA-treated OR rats on the 10% safflower diet. These differences were not seen in the OP strain. Gene expression analysis of mammary ductal epithelium from OR rats on the high fat diet showed significant upregulation of proliferation-related genes compared to those consuming the low fat safflower diet. Again, these differences were not seen in the OP strain. Conclusion: Our findings indicate that consumption of high fat safflower diet enhances mammary carcinogenesis in an OR rat strain through increased proliferation of mammary epithelium at the time of exposure, but not in the OP rat strain. Thus, the diet-induced increase in sensitivity was strain-specific and independent of weight gain or obesity level. Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly.
2010-09-25 | E-GEOD-21150 | biostudies-arrayexpress
Project description:Background: This study examines the impact of dietary fatty acids on regulation of gene expression in the mammary epithelial cells before and during puberty. Methods: The diets primarily consisted of n-9 monounsaturated fatty acids (olive oil), n-6 polyunsaturated fatty acids (safflower), saturated acids (butter), and the reference AIN-93G diet (soy oil). The dietary regimen mimics the repetitive nature of fatty acid exposure in Western diets. Dietary-induced changes in gene expression were examined in the LCM (Laser Capture Microdissected) captured mammary ductal epithelial cells at day of weaning (21 days) and at the end of puberty (50 days after birth). PCNA immunohistochemistry analysis was used to compare proliferation rates between diets. Results: Genes differentially expressed between each of the test diets and the reference diet in both age groups were significantly enriched by cell cycle genes. Some of these genes were involved in the activation of the cell cycle pathway or the G2/M check point pathway. Although there were some differences in the level of differential expression, all diets showed qualitatively same pattern of differential expression compared to the reference diet. Cluster analysis identified an expanded set of cell cycle as well as immunity and sterol metabolism related clusters of differentially expressed genes. Conclusion: Fatty acid-enriched diets significantly up-regulated proliferation above the normal physiological level at day 50. The higher cellular proliferation during puberty caused by enriched fatty acid diets pose a potential increase risk of mammary cancer in later life. The human homologs of 27 of 62 cell cycle cluster of rat genes are included in a human breast cancer cluster of 45 cell cycle related genes further emphasizing the importance of our findings in the rat model. Female, virgin Spraque-Dawley rats were obtained from Taconic Farms (Germantown, NY) at approximately 7 weeks of age and placed on one of 9 pelleted purified diets for one month. After one month of diet exposure, female rats were bred with male Sprague-Dawley rats of approximately 3 months of age. Litters were weighed and monitored throughout gestational period. Pups had access to dam’s milk as well as tap water and food throughout gestation. Pups were weaned at DOL 21 and individually housed with tap water and diets ad libitum. Rats were killed by CO2 asphyxiation and decapitated at the following two ages, DOW (DOL21) and DOL 50 with no other treatments.
2009-04-01 | E-GEOD-14933 | biostudies-arrayexpress
Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.
2014-10-25 | E-GEOD-62715 | biostudies-arrayexpress
Project description:To model the potential diabetogenic effects of higher level of HSD11B1 in b-cells of the pancreas in vivo, we created a transgenic model overexpressing HSD11B1 under the mouse insulin I promoter (MIP-HSD1) in diabetes-prone C57Bl/KsJ mice. KsJ wild type and MIP-HSD1 heterozygous mice have been high fat fed for 12 weeks. Pancreata have been perfused with collagenase and islets isolated by hand picking. Isolated islets (around 500) coming from at least 3 mice (around 200/mice) have been directly lysed in Trizol. Total RNA have been extracted by Trizol plus RNA Purification Kit (invitrogen). Four biological replicates per group: Wild type KsJ mice on High Fat diet (KsJ1, KsJ2, KsJ3, KsJ4) and MIP-HSD1 transgenic mice on High Fat diet (MIP1, MIP2, MIP3, MIP4) were used to prepare RNA for microarray analysis.
2011-06-30 | E-GEOD-23161 | biostudies-arrayexpress
Project description:This animal study was approved by the Ethics Committee at school of Chinese medicine,Hong Kong Baptist University. A total of 4 female and 4 male C57BL/6 mices were included in control diet group (BC); A total of 4 female and 4 male C57BL/6 mices were included in high fat diet group (BT).
2024-02-27 | PXD041294 | Pride
Project description:The effect of high fat diet feeding on heart gene transcription regulation was investigated in an F2 cross of 129S6 x Balb/c mice using Illumina gene expression arrays. Expression data was determined in 5 months old male mice fed a high fat diet (40% fat) for 15 weeks. Control mice were fed a standard carbohydrate chow. 96 animals per group were used. The files mouse-f2-chd-genotype.txt and HFD.txt contain genotyping data linked to the diets, they can be found found in the file E-MTAB-401.additional.zip on the FTP for this submission. NOTE: the file CHD.txt was replaced by the updated file mouse-f2-chd-genotype.txt on 8th April 2014.
2011-09-17 | E-MTAB-401 | biostudies-arrayexpress
Project description:We fed hypercholesterolemic mice high fat diet containing either ticagrelor, clopidogrel, or nothing (control) for 16 weeks, isolated the liver, extracted RNA, and subjected the RNA to RNA-Seq using NGS.
2019-06-16 | E-MTAB-8049 | 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:To identify molecular mechanism underlying the protection from diet-induced hepatic steatosis in AHNAK deficiency mice, we examined microarray analysis with liver sample from HFD-fed AHNAK KO and WT mice. Two-condition experiment, regular chow (CD) -fed WT vs. CD-fed AHNAK KO and High fat diet(HFD)-fed WT vs. HFD-fed AHNAK KO mice. Biological replicates: 3 control, One replicate per array.
2015-06-23 | E-GEOD-70119 | biostudies-arrayexpress
Project description:Background: Epidemiological studies suggest an association between maternal obesity and adverse neurodevelopmental outcomes in offspring. Objective: To compare the global proteomic portrait in the cerebral cortex between mice born to mothers on a high-fat or control diet who themselves were fed a high-fat or control diet. Methods: Male mice born to dams fed a control (C) or high fat (H) diet four weeks before conception and during gestation and lactation were assigned to either C or H diet at weaning. Mice (n=24) were sacrificed at 19-weeks and their cerebral cortices were pooled into 8 samples and analysed using an iTRAQ based 2D LC-MS methodology. Results: A total of 6,695 proteins were identified and fully quantified (q<0.01). Approximately 10% of these proteins demonstrated a minimum of one Standard Deviation of regulation across all biological replicates in at least one of the experimental groups (CH, HC, HH) relative to the control (CC). Principal component analysis and hierarchical clustering analysis showed that mice clustered based on the diet of the mother and not their current diet. In silico bioinformatics analysis revealed that maternal high-fat diet was significantly associated with response to hypoxia/oxidative stress and apoptosis in the cerebral cortex of the adult offspring. Conclusion: Maternal high-fat diet was associated with distinct endophenotypic changes of the adult mouse cerebral cortex independent of the diet of the offspring. The identified modulated proteins could represent novel therapeutic targets for the prevention of neuropathological features resulting from maternal obesity.
2018-01-29 | PXD001540 | Pride