Ontology highlight
ABSTRACT:
PROVIDER: PRJNA716417 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14038855_1.fastq.gz | Fastqsanger.gz | |||
| SRR14038855_2.fastq.gz | Fastqsanger.gz | |||
| SRR14038856_1.fastq.gz | Fastqsanger.gz | |||
| SRR14038856_2.fastq.gz | Fastqsanger.gz | |||
| SRR14038857_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of gene expression profiles of epididymal fat from DIO rats We applied a comparative functional genomics approach to evaluate diet-induced obese (DIO) rats as an obesity model Keywords: single time point, comparison control animal vs. diet induced obese animal
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Project description:To identify key biological pathways that define susceptibility factors for pulmonary infection during obesity, diet-induced obese (DIO) and regular weight (RW) C57BL/6 mice were exposed to 0.5 M-BM-5g/L inhaled lipopolysaccharide (LPS) for 1 hr/d for 4 days over a period of 2 weeks. Transcriptional responses were measured by global microarray analysis of lung tissue. Groups (N=8 biological replicates) of regular weight (RW) and diet-induced obese (DIO) C57BL/6 mice (15-weeks old at start of exposures) were exposed to either filtered air (sham controls, SC) or 0.5 M-BM-5g/L LPS by nose-only inhalation exposure for 1 hr/day for 4 days over a 10-day period with necropsies occurring on the day following the last exposure (Day 11).
2012-09-15 | E-GEOD-38092 | biostudies-arrayexpress
Project description:The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) increases with age and obesity. The aim of this study is to characterize the transcriptomic changes in liver underlying the beneficial effects of docosahexaenoic acid (DHA) supplementation on MASLD progression in aged obese female mice. Two-month-old C57BL/6J female mice were fed ad libitum with high fat saturated diet (HFD, 45%) for 4 months. These diet-induced obese (DIO) mice were divided into two groups: the DIO group that continued with HFD and the DIO + DHA mice fed up to 18 months with the HFD containing a DHA-rich concentrate. High quality RNA from liver was used to perform RNA sequencing analysis. Further functional and clustering analyses of differentially expressed genes (DEGs) in liver between treatments revealed that DHA regulated processes related to lipid metabolic processes such as fatty acid beta oxidation, lipid storage, fatty acid transport and lipid localization. DHA treatment also affects PPAR signaling pathway and the regulation of inflammatory response. These data suggest that long-term DHA supplementation ameliorates MASLD progression in aged obese female mice by promoting transcriptomic changes in genes related to lipid metabolism and inflammatory response.
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Project description:To profile the expression of circulating miRNAs in a mouse model of diet-induced obesity (DIO) with subsequent weight-reduction with low-fat diet (LFD), eighteen C57BL/6 male mice were grouped into three subgroups as: (1) Control: the mice fed with the standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice fed with 58 kcal% high-fat diet for 12 wks; (3) DIO+LFD: the mice fed with high-fat diet for 8 wks to induce obesity, then changed to 10.5 kcal% low-fat diet for subsequent 4 wks. C57BL/6 mice were purchased from BioLasco (Taipei, Taiwan). All housing conditions were maintained, and surgical procedures, including analgesia, were performed in an Association for Assessment and Accreditation of Laboratory Animal Care International (AAALAC)-accredited SPF facility according to national and institutional guidelines. In this experiment, eighteen C57BL/6 wild type male mice were randomly grouped into three subgroups (n=6 in each group): (1) Control: the control mice were fed ad libitum a standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice were fed ad libitum a 58 kcal% HFD (D12331; Research Diets Inc., New Brunswick, NJ) for 12 wks to induce obesity; (3) DIO+LFD: the mice fed ad libitum a 58 kcal% HFD (D12331) for 8 wks to induce obesity, then continued the feeding of 10.5 kcal% LFD (D 12329; Research Diets Inc.) for additional 4 wks. Weight measurements were performed on a weekly basis to for these three groups of mice. Evaluation of blood glucose levels was performed at the beginning and in the end of the experiment to confirm that the HFD-fed mice developed an obese and insulin resistant phenotype. After the end of experiment at 12w, all mice were killed. The abdominal WAT of each mice was removed and weighted. Paraffin-embedded abdominal WAT was sectioned at 5 M-NM-<m and stained with hematoxylin and eosin to measure mean adipocyte area. A volume of 1 mL of whole blood was collected into a plain tube and allowed to clot for 1 hour. The sera samples were aliquoted after centrifugation at 3,000 M-CM-^W g for 10 minutes and stored at M-bM-^HM-^R80M-BM-0C until further analysis.
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Project description:Roux-en-Y gastric bypass (RYGB) is the most effective therapy for morbid obesity, but it has a ~20% failure rate. We used our established RYGB model in diet-induced obese (DIO) Sprague-Dawley rats, which reproduces human bi-phasic body weight (BW) loss pattern, to determine mechanisms contributing to success (RGYB-S) or failed (RYGB-F) RYGB. DIO rats were randomized to RYGB, sham operated Obese, and sham operated obese pair fed-linked to RYGB (PF) groups. BW, caloric intake (CI) and fecal output (FO) were recorded daily for 90 days, food efficiency (FE) was calculated, and morphologic changes were determined. Gut, adipose and thyroid hormones were measured in plasma. Mitochondrial respiratory complexes in skeletal muscle, expression of energy-related hypothalamic and fat peptides, receptors and enzymes were quantified. A 25% failure rate occurred. RYGB-S, RYGB-F and PF rats vs. Obese showed rapid BW decrease, followed by sustained BW loss in RYGB-S. RYGB-F and PF gradually increased BW. Expression profiling of both CNS (hypothalamus) and peripheral tissues (subcutaneous abdominal fat) strongly supported the involvement of a number of metabolic and feeding-related genes in the differential outcomes. Experiment Overall Design: 3 biological replicate RNA samples were prepared from 2 tissues (the subcutaneous abdominal fat or the hypothalamus) from rats in 3 treatment groups (rats losing weight successfully after gastric bypass surgery, rats gaining weight, and rats that were fed the same amount as the treated rats)
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Project description:To profile the expression of circulating miRNAs in a mouse model of diet-induced obesity (DIO) with subsequent weight-reduction with low-fat diet (LFD), eighteen C57BL/6 male mice were grouped into three subgroups as: (1) Control: the mice fed with the standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice fed with 58 kcal% high-fat diet for 12 wks; (3) DIO+LFD: the mice fed with high-fat diet for 8 wks to induce obesity, then changed to 10.5 kcal% low-fat diet for subsequent 4 wks.
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Project description:Roux-en-Y gastric bypass (RYGB) is the most effective therapy for morbid obesity, but it has a ~20% failure rate. We used our established RYGB model in diet-induced obese (DIO) Sprague-Dawley rats, which reproduces human bi-phasic body weight (BW) loss pattern, to determine mechanisms contributing to success (RGYB-S) or failed (RYGB-F) RYGB. DIO rats were randomized to RYGB, sham operated Obese, and sham operated obese pair fed-linked to RYGB (PF) groups. BW, caloric intake (CI) and fecal output (FO) were recorded daily for 90 days, food efficiency (FE) was calculated, and morphologic changes were determined. Gut, adipose and thyroid hormones were measured in plasma. Mitochondrial respiratory complexes in skeletal muscle, expression of energy-related hypothalamic and fat peptides, receptors and enzymes were quantified. A 25% failure rate occurred. RYGB-S, RYGB-F and PF rats vs. Obese showed rapid BW decrease, followed by sustained BW loss in RYGB-S. RYGB-F and PF gradually increased BW. Expression profiling of both CNS (hypothalamus) and peripheral tissues (subcutaneous abdominal fat) strongly supported the involvement of a number of metabolic and feeding-related genes in the differential outcomes. Keywords: gene expression analysis
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