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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse model of obesity during high fat feeding

ABSTRACT: We examined the effects of high-fat diet on feeding behaviour, body weight regulation and common biomarkers associated with weight gain in the C57BL/6J mice over a period of 10 weeks, making measurements at weeks 2, 4 and 10. We examined the transcriptomic profile of hepatic genes involved in the major lipid metabolic pathways, validating the key genes with quantitative real-time reverse-transcription PCR (qRT-PCR) and their gene products with western blots. Experiment Overall Design: C57BL/6J mice were randomly assigned to consume either the control (C) or HFC diet. Body weights and food intake were measured weekly and other measurements at weeks 2, 4 and 10. Microarrays were used to screen the transcriptional response of the livers at the 3 time-points. Genes, encoding enzymes regulating key steps of lipid metabolism, were then selected from the microarray data for validation by qRT-PCR and their protein expression by western blot assays.

ORGANISM(S): Mus musculus

SUBMITTER: Mei Yen Chan

PROVIDER: E-GEOD-8753 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Sequential responses to high-fat and high-calorie feeding in an obese mouse model.

Chan Mei-Yen MY Zhao Yulan Y Heng Chew-Kiat CK

Obesity (Silver Spring, Md.) 20080221 5

<h4>Objective</h4>Reports on the immediate and long-term responses to high-fat and high-calorie (HFC) feeding are controversial. Therefore, we examined the sequential effects of an HFC diet.<h4>Methods and procedures</h4>C57BL/6J mice were randomly assigned to consume either the control (C) or the HFC diet. Body weights and food intake were measured weekly and other measurements at weeks 2, 4, and 10. Microarrays were used for screening the transcriptional response of the livers at the three tim ...[more]

PMID: 18292748

Similar Datasets

Sequential responses to high-fat feeding in an obese mouse model

Project description:We examined the effects of high-fat diet on feeding behaviour, body weight regulation and common biomarkers associated with weight gain in the C57BL/6J mice over a period of 10 weeks, making measurements at weeks 2, 4 and 10. We examined the transcriptomic profile of hepatic genes involved in the major lipid metabolic pathways, validating the key genes with quantitative real-time reverse-transcription PCR (qRT-PCR) and their gene products with western blots. Keywords: Lipogenesis, Hyperphagia, Fat Oxidation, Energy Regulation, Body Weight

2007-12-01 | GSE8753 | GEO

transcription profiling by array of C57BL/6J mice fed a Western-style diet with or without 0.05% quercetin against mice on a control diet to study the effect of quercetin on obesity and hepatic gene expression

Project description:To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression, C56BL/6J mice were fed for 20 weeks on control or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Chronic dietary intake of quercetin reduced body weight gain and visceral and liver fat accumulation, and improved hyperglyceamia, hyperinsulinaemia, dyslipidaemia in mice fed a Western-style diet. Feeding a Western-style diet altered expression of genes related to inflammatory responses, lipid metabolism and oxidative phosphorylation in C57BL/6J mice after 20 weeks. The results from exhaustive gene expression analysis showed that quercetin minimally influenced hepatic gene expression in mice fed the Western diet. The gene screening results (GSEA) were consistent with the notion that it did improve mitochondrial function to some extent. Quantitative RT-PCR analysis indicated that quercetin did influence important regulators of fat accumulation and metabolic disorders. Our results suggest that quercetin reduces fat accumulation presumably through decreasing oxidative stress and increasing PPARα expression, and the following improvement of gene expression related to steatosis in the liver. C56BL/6J mice were fed for 20 weeks on AIN93G (con) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin for 20 weeks.

2012-05-29 | E-GEOD-38141 | biostudies-arrayexpress

Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice

2012-05-30 | GSE38141 | GEO

Quercetin decreases high-fat diet induced bodyweight gain and accumulation of hepatic and circulating lipids in mice.

Project description:Dietary flavonoids are supposed to be protective against cardiovascular diseases (CVD). Elevated circulating lipid levels and hepatic lipid accumulation are known risk factors for CVD. We investigated the effects and underlying molecular mechanisms of the flavonoid quercetin on hepatic lipid metabolism in mice with diet induced body weight gain and hepatic lipid accumulation. Adult male mice received a high-fat diet without or with supplementation of 0.33% (w/w) quercetin for 12 weeks. Body weight gain was 29% lower in quercetin-fed mice (p<0.01), while the energy intake was not significantly different. Quercetin supplementation reduced hepatic lipid accumulation with 71% (p<0.05). 1H nuclear magnetic resonance serum lipid profiling revealed that the supplementation lowered serum lipids (p<0.0001). Global gene expression profiling of liver showed that key target genes of the transcription factor Constitutive androstane receptor (Car; official symbol Nr1i3) were regulated, in particular Cytochrome P450 2b (Cyp2b) genes. Quercetin can decrease high-fat diet induced body weight gain, hepatic lipid accumulation and serum lipid levels, which might be explained by the regulation of Cytochrome P450 genes under transcriptional control of CAR, an effect which is likely dependent on dietary background. Liver samples were obtained from 24 C57BL/6J male adult mice. All mice started with a three week adaptation phase, in which they were fed a normal-fat diet. During the intervention of 12 weeks, the mice received a high-fat diet without (HF) or with supplementation of 0.33% (w/w) quercetin (HF-Q). Based on visual inspection, three arrays lacked homogenous hybridization and were therefore excluded.

2014-10-14 | E-GEOD-51343 | biostudies-arrayexpress

Consequences of exchanging carbohydrates for proteins in the cholesterol metabolism of mice fed a high-fat diet

Project description:Dietary proteins have profound effects on lipid metabolism but the mechanism remains to be elucidated. In the present study, we examined the temporal impact of dietary proteins in isoenergetic high fat diets on lipid metabolism of C57BL/6J mice. Mice were first fed a low protein (P) to carbohydrate (C) ratio high-fat diet (L-P/C-HF) for 10 weeks and then a half of mice were changed to a high protein to carbohydrate ratio high-fat diet (H-P/C-HF) for additional 4 weeks whereas the remaining mice continued eating the L-P/C-HF diet.

2012-12-19 | E-GEOD-20260 | biostudies-arrayexpress

Proteomics analysis of insulin sensitive tissues in high fat diet fed mice

Project description:The popularity of high fat foods in modern society has been associated with epidemic of various metabolic diseases characterized by insulin resistance, the pathology of which involves complex interactions between multiple tissues such as liver, skeletal muscle and white adipose tissue (WAT). To uncover the mechanism by which excessive fat impairs insulin sensitivity, we conducted a multi- tissue study by using TMT-based quantitative proteomics. 3-week-old ICR mice were fed with high fat diet (HFD) for 19 weeks to induce insulin resistance. Liver, skeletal muscle and epididymal fat were collected for proteomics screening. Additionally, PRM was used for validating adipose differential proteins. By comparing tissue-specific protein profiles of HFD mice, multi-tissue regulation of glucose and lipid homeostasis and corresponding underlying mechanisms was systematically investigated and characterized. NC: normal birth weight + chow diet; NH: normal birth weight + high fat diet; LC: low birth weight + chow diet; LH: low birth weight + high fat diet.

2022-01-26 | PXD021046 | Pride

Proteomics reveals PFOS-induced alteration of lipid utilization and xenobiotic metabolism in a model of PFOS-augmented diet-induced fatty liver

Project description:Perfluorooctanesulfonic acid (PFOS) is a persistent, bio-accumulative pollutant that has been used for the last 60+ years in numerous industrial and commercial applications. In mice, PFOS administration is known to induce hepatomegaly and hepatic steatosis. The aim of the present study was to evaluate potential PFOS and diet interactions and explore the mechanism of PFOS induced liver lipid accumulation. Prior to PFOS administration, mice were fed either a standard chow diet (SD) or 60% kCal high fat diet (HFD) for 4 weeks to establish significant body weight increase. After 4 weeks of diet acclimation, the treatment groups received 0.0003% PFOS in diet for an additional 10 weeks. In addition, a subset of the mice fed HFD were switched to a SD (H-SD) to mimic weight-loss induced improvement of hepatic steatosis. A total of six treatment groups: i) SD, ii) HSD, iii) HFD (H), iv) SD +PFOS(SDP), v) H-SD +PFOS (HSDP), and vi) HFD +PFOS (HP) were included. PFOS and lipid concentrations were measured in both serum and liver. Relative liver mRNA expression was determined by targeted bead array and proteins were quantified using untargeted mass spectrometry. PFOS exposure increased liver weight, and in the HFD increased liver triglycerides and liver cholesterol content. Gene and protein expression in the liver demonstrated that PFOS exposure induced lipid utilization and xenobiotic metabolism pathways, and in a HFD, induced lipid synthesis. The data suggests that PFOS exposure acts on lipid utilization genes and exacerbates hepatic steatosis in mice fed a HFD.

2020-09-30 | PXD016161 | Pride

XX chromosome complement promotes, and w-3 fatty acid treatment prevents, adverse statin effects in mice

Project description:RNA-sequening of livers from male and female C57BL/6J mice fed either chow diet or chow diet + simvastatin (0.1g/kg body weight) for 4 weeks.

2024-02-01 | GSE184588 | GEO

Expression data from Control diet, Western diet and Western diet + DHA fed rats.

Project description:LV hypertrophy is associated with Western diet consumption, while intake of n-3 polyunsaturated fatty acids is associated with anti-hypertrophic effects. We treated rats for 12 weeks with either a Control diet, a Western diet or a Western + DHA diet. For each of the 3 dietary treatments there were 2 pooled samples of heart tissue (with each pooled sample representing 5 rats) for a total of 6 arrays. Microarray analysis identified 66 differentially expressed transcripts. Pathways were identified using Ingenuity and DAVID software. Array results from two pooled samples (5 rats in each pool) for n=10 per treatment group were used for comparisons. Comparisons between Western vs. Control, Western + DHA vs. Control and Western + DHA vs. Western diets was subjected to analysis to generate log fold changes. A dietary treatment of 12 weeks was used in an effort to produce LVH while limiting the development of comorbidities. Microarray analysis was performed on pooled samples, followed by qRT-PCR and Western blot analysis. Groups were Control, Western and Western + DHA. Comparisons between groups are expressed as LogFC (i.e. LogFC_WESvCTRL, LogFC_DHAVCTRL, LogFC_DHAvWES), available in Series supplementary files.

2013-11-22 | E-GEOD-52603 | biostudies-arrayexpress

Gene expression profiles of livers and liver tumors from mice fed high-fat diet and high fructose-glucose solution for 52 weeks

Project description:The lack of a preclinical model of nonalcoholic steatohepatitis (NASH) and hepatocellular cancer (HCC) that recapitulates human disease is a major barrier to therapeutic development. We report a high fat-high sugar diet-induced NASH and HCC in a stable isogenic 129S1/SvImJ crossed with C57Bl/6J mice. Following diet initiation, there was sequential development of steatosis (4-8 weeks), steatohepatitis with ballooning and Mallory-Denk bodies (12-16 weeks), progressive fibrosis (16 week onwards) and spontaneous HCC (32-52 weeks). The mice developed obesity, insulin resistance and dyslipidemia. There was concordance with the human NASH transcriptome (FDR 0.001) with activation of lipogenic, inflammatory and apoptotic pathways relevant in humans. The HCC gene signature resembled S1 and S2 human HCC subclass (FDR 0.01 for both). This simple model of NASH and HCC that resembles human disease in terms of its triggers, physiological and biochemical parameters, histology, transcriptomic profile, and outcomes can facilitate preclinical development for these conditions. 129S1/SvImJ;C57Bl/6J (129/B6) mice were fed with high-fat diet (Western Diet) and high fructose-glucose solution (Sugar Water) (WD SW) or chow diet (CD) for 52 weeks, and total RNA samples were isolated from liver and tumor tissues for genome-wide expression profiling.

2016-07-25 | E-GEOD-67679 | biostudies-arrayexpress

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