Mus musculus
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-38136
PROVIDER: PRJNA167275 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatic gene expression in streptozotocin-induced diabetic mice fed a quercetin diet
| PRJNA167181 | ENA
Project description:We showed that diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a). In this experiment, we determined the effect of quercetin on healthy control BALB/c mice that were fed the AIN93G diet containing 0, 0.1, 0.5 or 1% quercetin for 2 weeks. GSEA and one-way ANOVA did not detect any significant changes in hepatic gene expression in normal mice as a result of a quercetin diet. Using a linear modeling approach and the empirical Bayes statistics, we found that Ubc were significantly reduced by both the 0.5% and 1% quercetin. Six-week-old male mice were divided into 4 groups of 6 mice each, housed in groups of 3 per cage, and fed a standard purified AIN-93G diet containing 0% (Control), 0.1% (0.1), 0.5% (0.5), or 1% quercertin (1.0) for 2 weeks.
2012-05-29 | E-GEOD-38136 | biostudies-arrayexpress
Project description:We showed that diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a). In this experiment, we determined the effect of quercetin on healthy control BALB/c mice that were fed the AIN93G diet containing 0, 0.1, 0.5 or 1% quercetin for 2 weeks. GSEA and one-way ANOVA did not detect any significant changes in hepatic gene expression in normal mice as a result of a quercetin diet. Using a linear modeling approach and the empirical Bayes statistics, we found that Ubc were significantly reduced by both the 0.5% and 1% quercetin.
2012-05-30 | GSE38136 | GEO
Project description:Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)-induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes-associated liver injury. We fed STZ-induced diabetic mice with diets containing 0.1% or 0.5% quercetin for 2 weeks and compared the patterns of hepatic gene expression in these groups of mice using a DNA microarray. Diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a).
2012-05-23 | GSE38067 | GEO
Project description:Hepatic gene expression in BALB/c mice fed a quercetin diet
2014-10-10 | E-GEOD-38136 | ExpressionAtlas
Project description:Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)-induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes-associated liver injury. We fed STZ-induced diabetic mice with diets containing 0.1% or 0.5% quercetin for 2 weeks and compared the patterns of hepatic gene expression in these groups of mice using a DNA microarray. Diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a). Six-week-old male mice were divided into 4 groups of 6 mice each, housed in groups of 3 per cage. After 1 week mice were intraperitoneally injected with STZ. Mice (n=6) in the untreated control group did not receive any treatment. After 1 week, 18 mice showing non-fasting blood glucose levels of 230-400 mg/dL were divided into 3 groups: one group was fed with AIN93G only (control group), the others with an AIN93G diet containing 0.1% or 0.5% quercetin (Funakoshi, Tokyo, Japan) for 2 weeks.
2012-05-22 | E-GEOD-38067 | biostudies-arrayexpress
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
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.
2012-05-30 | GSE38141 | GEO
Project description:Hepatic gene expression in C56BL/6J mice fed a quercetin diet for 20 weeks
| PRJNA265188 | ENA
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