Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA300676 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 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.
2014-09-03 | GSE61005 | GEO
Project description:To assess changes in expression level of various chemokines and their receptors on diet-induced obesity, we analysed gene expression in adipose tissue of C56BL/6J mice fed a high-fat (HF) diet or normal chow diet for 8 weeks. HF diet-induced obese (DIO) mice showed adipose tissue inflammation and insulin resistance. Comprehensive gene expression analysis showed that MCP-1–CCR2 and CCL5–CCR5 signalling in epididymal white adipose tissue (eWAT) were enhanced during the development of obesity. Surprisingly, the gene expression of Cx3cl1 was decreased in the eWAT of DIO mice compared with lean mice. While Cx3cr1 expression showed no significant difference between DIO and lean mice. Decreased CX3CL1-CX3CR1 signalling in adipose tissue may also be involved in the development of obesity-induced adipose tissue inflammation and insulin resistance.
2021-04-01 | GSE167311 | GEO
Project description:High-fat diet (HFD) induced obesity (DIO) has been shown impacts on metabolism, hormonal profile, male fertility, and spermatogenesis. We employed genome-wide transcriptional analysis on the testis of diet induced obesity (DIO) and normal chow (NC) C57BL/6 J male mice to search genes regulated by obesity in testis. Both blood glucose and lipids contents significantly increased in DIO mice after 8 weeks fat-rich feeding. RNA-seq analysis revealed 371 down-regulated and 460 up-regulated transcripts in DIO group comparing to NC group. Chromosome 3, 4, 9, 16, and 18 were significantly more active, while chromosome 5, 10, and 19 were significantly more inactive after 8-week fat-diet feeding. Wilcoxon enrichment analysis discovered that the thermogenesis pathway (KEGG) was significantly enriched in the testis of DIO group (with 8 enriched up-regulated genes: Smarca2, Adcy3, Atp5pb, Creb1, Gnas, Rps6kb2, Upcrc1 and Dpf1). Real-time PCR further confirmed that Smarca2 and Atp5pb were upregulated in the testis of DIO mice. These finding implied that diet-induced thermogenesis pathways could be altered in the testis of DIO mice.
2023-02-04 | GSE196119 | GEO
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: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.
2014-09-03 | E-GEOD-61005 | biostudies-arrayexpress
Project description:Investigating alterations the intestinal microbiome in a diet induced obesity (DIO) rat model after fecal transplant from rats, which underwent Roux-Y-Gastric-Bypass surgery (RYGB). The microbiomes of the RYGB-donor rats, the DIO rats, and DIO rats after receiving the fecal transplant from the RYGB rats. As controls lean rats as well as lean, RYGB and DIO rats after antibiotics treatment were used.
2022-08-12 | PXD026606 | Pride
Project description:ApoA-IV produced by enterocytes as a major component of high-density lipoprotein plays a role in the satiation signal and also the transport of serum lipids. The present study aimed to investigate the effects of ApoA-IV on diet-induced obesity (DIO), metabolic inflammation and the underlying mechanisms. C57BL/6J ApoA-IV-/- (KO) and wildtype (WT) mice as well as KO mice stably transfected with ApoA-IV-green fluorescent protein (KO-A4-GFP) or solely GFP (KO-GFP) encoding adenoviruses were fed with standard 5% fat rodent chow (CD) or 60% high fat rodent chow (HFD) for 16 weeks.
2022-10-25 | GSE211980 | GEO
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
2007-08-07 | GSE8700 | GEO
Project description:Obesity leads to ovarian dysfunction and the establishment of local leptin resistance. The aim of our study was to characterise levels of Nod-Like Receptor Protein 3 (NLRP3) inflammasome activation during obesity progression in the mouse ovaries and liver and test the putative role of leptin on its regulation. C57BL/6J mice were treated with equine chorionic gonadotropin (eCG) or human chorionic gonadotropin (hCG) for oestrous cycle synchronisation and ovaries collection. In diet-induced obesity (DIO) model, mice were fed chow diet (CD) or high fat diet (HFD) for 4 or 16 weeks (wk), whereas in hyperleptinemic model (LEPT), mice were injected with leptin for 16 days (16L) or saline (16C) and in the genetic obese leptin-deficient ob/ob (+/? and -/-) animals were fed CD for 4wk. Either ovaries and liver were collected, as well as cumulus cells (CCs) after superovulation from DIO and LEPT. In DIO protocol, protein expression of NLRP3 inflammasome components was increased in 4wk HFD, but decreased in 16wk HFD. Moreover LEPT and ob/ob models revealed NLRP3 and IL-1 upregulation in 16L and downregulation in ob/ob. Transcriptome analysis of CC showed common genes between LEPT and 4wk HFD modulating NLRP3 inflammasome. Moreover analysis in the liver showed upregulation of NLRP3 protein only after 16wk HFD, but also the downregulation of NLRP3 protein in ob/ob-/-. We showed the link between leptin signalling and NLRP3 inflammasome activation in the ovary throughout obesity progression in mice, elucidating the molecular mechanisms underpinning ovarian failure in maternal obesity.
2021-11-01 | GSE180300 | GEO