Ontology highlight
ABSTRACT:
PROVIDER: PRJNA622821 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11472400.fastq.gz | Fastqsanger.gz | |||
| SRR11472500.fastq.gz | Fastqsanger.gz | |||
| SRR11472600.fastq.gz | Fastqsanger.gz | |||
| SRR11472700.fastq.gz | Fastqsanger.gz | |||
| SRR11472401.fastq.gz | Fastqsanger.gz |
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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:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study Nine-week-old C57Bl/6J mice were fed a low-fat diet (LF-PO) and three different types of high-fat diet, based on palm oil (HF-PO; P/S1.0), olive oil (HF-OO; P/S4.6) and safflower oil (HF-SO; P/S10.1) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. After 2 weeks of diet intervention, 6 mice per high-fat diet group were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%) and the small intestines were excised. Adhering fat and pancreatic tissue were carefully removed. The small intestines were divided in three equal parts along the proximal to distal axis (SI 1, SI 2 and SI 3) and microarray analysis was performed on mucosal scrapings.
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2014-03-01 | E-GEOD-39549 | biostudies-arrayexpress
Project description:Germfree (GF) mice have been used as a model to study the contribution of the intestinal microbiota to metabolic energy balance of the host. Despite a wealth of knowledge accumulated since the 1940’s, the response of GF mice to a high fat diet is largely unknown. In the present study, we compared the metabolic consequences of a high fat (HF) diet on GF and conventional (Conv) C57BL/6J mice. As expected, Conv mice developed obesity and glucose intolerance with a HF diet. In contrast, GF mice remained lean and resisted the HF diet-induced insulin resistance. The anti-obesity phenotype of GF/HF mice was accompanied by reduced caloric intake, diminished food efficiency, and excessive fecal lipid excretion contributed to the reduced food efficiency. In addition, HF diet-induced hypercholesterolemia was ameliorated, which was partially due to an increase in fecal cholesterol excretion. However, hepatic cholesterols were increased in GF/HF mice. Elevated nuclear SREBP2 proteins and the up-regulation of cholesterol biosynthesis genes support the increased liver cholesterol biosynthesis in GF/HF mice. The resistance to HF diet-induced metabolic abnormalities in GF mice was also associated with a reduced immune response, indicated by low plasma pro-inflammatory and anti-inflammatory markers. These data suggest that the gut microbiota of Conv mice contributes to HF diet-induced obesity, insulin resistance, dyslipidemia and hepatic steatosis in mice. Thus, results of the present study describe the metabolic responses of GF mice to a HF diet and further our understandings of the relationship between the gut microbiota and the host. Germfree and conventional C57BL/6J mice were fed with a high fat diet for 11 weeks. Then, all mice were sacrified under 10-h food deprevation, and liver samples of germfree (n=14) and conventional (n=16) were examined.
2010-08-20 | E-GEOD-19038 | biostudies-arrayexpress
Project description:Obesity is a global health concern affecting over 650 million adults with a major contributor being an increased consumption of a high-fat diet. Maternal obesity often results in an increased risk of offspring developing obesity. In this study, we examined the effect of diet on visceral adipose in a pre-clinical model of generational diet-induced obesity that included maternal cohorts of C57BL/6 mice fed either a control diet (10% fat) or a high-fat diet (45% fat) and the resulting female offspring fed either diet. Using bottom-up proteomics on omental adipose tissue, differential protein expression was determined with the greatest difference resulting from the generational obese cohort. Differentially expressed proteins were involved in pathways related to cancer, inflammatory disease and immune response. Taken together, the results of this study provide molecular-level insight that will enable the development of more targeted, modifiable interventions that could be implemented pre-, during and post-pregnancy.
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Project description:Obesity alters the transcriptional profile of the adipose tissue. Our aim was to characterize the metabolic adaptations induced by diet-induced obesity in the adipose tissue. To this end wild-type mice were fed for 20 weeks a high-fat diet and subcutaneous adipose tissue was analyzed by RNA sequencing.
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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:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study
2012-06-18 | GSE18586 | GEO