Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA113095 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Increasing the consumption of dietary fibre has been proposed to alleviate the progression of non-communicable diseases such as obesity, type 2 diabetes and cardiovascular disease, yet the effect of dietary fibre on host physiology remains unclear. In this study, we performed a multiple diet feeding study in C57BL/6J mice to compare high fat and high fat modified with dietary fibre diets on host physiology and gut homeostasis by combining proteomic, metagenomic, metabolomic and glycomic techniques with correlation network analysis. We observed significant changes in physiology, liver proteome, gut microbiota and SCFA production in response to high fat diet. Dietary fibre modification did not reverse these changes but was associated with specific changes in the gut microbiota, liver proteome, SCFA production and colonic mucin glycosylation. Furthermore, correlation network analysis identified gut bacterial-glycan associations.
2021-09-08 | PXD014132 | Pride
Project description:The C57BL/6J mouse model develops obesity and pre-diabetes when fed a high-fat diet. In this experiment, DNA methylation was assessed globally at specific CpG sites in liver tissue from mice receiving high-fat diet (45E% from fat) for 13 weeks (Control) or high-fat diet supplemented with 20% (w/w) of freeze-dried lingonberries (n=4). Our findings show that lingonberries prevent development of high-fat induced obesity, hepatic steatosis and low-grade inflammation, and the DNA was hypermethylated in mice receiving lingonberries compared to control. Genome wide hepatic DNA methylation comparison between mice fed high-fat diet with or without a lingonberry supplement (n=4/group).
2015-09-20 | E-GEOD-67277 | biostudies-arrayexpress
Project description:The C57BL/6J mouse model develops obesity and pre-diabetes when fed a high-fat diet. In this experiment, DNA methylation was assessed globally at specific CpG sites in liver tissue from mice receiving high-fat diet (45E% from fat) for 13 weeks (Control) or high-fat diet supplemented with 20% (w/w) of freeze-dried lingonberries (n=4). Our findings show that lingonberries prevent development of high-fat induced obesity, hepatic steatosis and low-grade inflammation, and the DNA was hypermethylated in mice receiving lingonberries compared to control.
2015-09-20 | GSE67277 | GEO
Project description:Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. Keywords: response to high fat diet
2008-02-28 | GSE10639 | GEO
Project description:Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time-course microarray analysis (8 time-points over 24 weeks) of high-fat diet fed mice compared to normal diet fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. When we merged core diet-induced obesity networks, Tlr2, Cd14 and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further protein-protein interaction network analysis revealed Tlr2, Cd14 and Ccnd1 were inter-related through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14 and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH. Total RNA obtained from isolated liver of C57BL/6J mice fed normal diet or high fat diet for 0, 2, 4, 6, 8, 12, 16, 20 and 24 weeks.
2014-03-01 | E-GEOD-40481 | biostudies-arrayexpress
Project description:Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. Experiment Overall Design: Microarray analyses were performed on quadruplicate RNA samples of pancreatic islets from AKR and Bl6 mice placed on high-fat diet for 3 months. Pancreases from two mice were combined to yield one sample of islet RNA. All protocols were conducted as described in the Affymetrix GeneChips Expression Analysis Technical Manual (Affymetrix, Santa Clara, CA) using 5 μg total RNA and GeneChip Mouse Expression Arrays MOE 430 (Affymetrix).
2008-04-07 | E-GEOD-10639 | biostudies-arrayexpress
Project description:Inbred C57BL/6J mice differ in their susceptibility to diet-induced obesity. Comparison of the liver transcriptomes leads to genes that are involved in the development as well as the maintenance of fatty liver during the onset of obesity upon high fat diet feeding. Genes being upregulated in DIO responder can be seen as drivers of fatty liver development, while genes upregulated in DIO non-responder are most likely involved in the protection against fatty liver diseases.
2018-10-30 | GSE74542 | GEO
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:The effect of dietary calcium and dairy proteins on adipose tissue gene expression profile in diet induced obesity Experiment Overall Design: 9-week-old C57Bl/6J-mice were divided into two groups (n=10/group). The control diet was a standard high-fat diet (60% of energy) low in calcium (0.4%). The whey protein diet was a high-calcium (1.8%) high-fat diet with whey protein isolate. After the 21-week treatment, the adipose tissue transcript profiling (2 mice/group) was carried out using Affymetrix Mouse Genome 430 2.0 array.
2008-04-07 | E-GEOD-9280 | biostudies-arrayexpress
Project description:Rodents respond to chronic high fat diet in at least two ways: some of them may readily gain body weight and become obese (termed obesity-prone), and others may not (termed obesity-resistant). An integrated approach of transcript and metabolic profiling of obesity-prone and obesity-resistant rats has been conducted, showing significantly different transcript and metabolic profiles in the two phenotypes. The major transcriptional differences involved hepatic fatty acid metabolism and ketogenesis in response to 16 weeks of high fat diet. At the same time, the different metabolic profiles (in liver tissue extracts, serum, and urine) between the two phenotypes could be ascribed to the corresponding pathways identified with multivariate statistical analysis, including fatty acid metabolism, Krebs cycle, and amino acid metabolism. The integration of results from both transcript and metabolic profiling revealed the different responses to dietary intervention of the two phenotypes and the physiological basis of susceptibility to metabolic disease in obesity-prone rats from a systematic view.
2008-05-20 | GSE11492 | GEO