Diffrential expression of adipose tissue immune cells after normal diet and high-fat diet induced obesity by RNA-seq analysis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE244406 | GEO | 2023/10/01
REPOSITORIES: GEO
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Project description:Obesity is tightly associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms of obesity-induced fatty liver remain largely unknown.In order to identify genes that are potentially involved in dysfunctional hepatic lipid homeostasis in obesity, we performed a clustering analysis of Affymetrix arrays,which revealed that a number of mRNAs were dys-regulated in the livers of mice fed a high-fat diet (HFD), compared with mice fed a normal chow diet (ND). To identify genes that are potentially involved in dysfunctional hepatic lipid homeostasis in obesity, male C57BL/6 mice aged 8 weeks were fed a normal diet (ND) or high-fat-diet (HFD) containing 60 Kcal% of fat for 12 weeks. Then mice were sacrificed and total RNAs were isoloated from hepatic tissues. Affymetrix array hybridisation and scanning were performed using Mouse Genome 430 2.0 chips.Total RNA samples obtained from six mice per group (ND and HFD) and pooled by each of the two were used for microarray analysis.
2014-05-09 | E-GEOD-57425 | biostudies-arrayexpress
Project description:Despite wide efforts in the last decade, signaling aberrations associated with obesity remain enigmatic. Here, we carried out phosphoproteomic analysis of mouse white adipose tissues (WAT) upon low-fat diet (LFD) and high-fat diet (HFD) to dissect underlying molecular mechanisms of obesity. Of the 7696 phosphopeptides quantified, 191 proteins including various insulin-responsive proteins and metabolic enzymes functioning in lipid homeostasis, exhibited differential phosphorylation with high-fat feeding. Kinase predictions and integrated network analysis identified several deregulated kinase signaling pathways, and suggested possibilities of HFD-induced transcriptional rewiring. Further, functional validation of a novel HFD-responsive site on cytoplasmic acetyl-coA forming ACSS2 (S263) suggested that the phosphorylation is important in regulating insulin signaling and maintaining triglyceride levels. This study represents one of the first comprehensive phosphoproteome data in mouse obesity models, and describes a systems-level approach for identifying deregulated molecular events and potential therapeutic targets in the context of high-fat feeding and adipocyte perturbation.
2016-05-20 | PXD002927 | Pride
Project description:Analysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions. GPR120 KO mice and the corresponding wild-type with normal diet(ND) or high fat diet(HFD), were subjected to Affymetrix Mus musculus microarrays. Epididymal adipose tissue and liver were analyzed in triplicates.
2012-02-22 | E-GEOD-32095 | biostudies-arrayexpress
Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.
2014-10-25 | E-GEOD-62715 | biostudies-arrayexpress
Project description:The High Fat Diet (HFD)-feeding significantly stimulated fat accumulation in Drosophila adults. Simultaneous feeding of known anti-obesity drugs that having the effect on rat and mouse, Quercetin Glycosides (QG) and Epigallocatechin gallate (EGCG) also suppressed fat accumulation in Drosophila at an equivalent concentration. Therefore, we have established a convenient model system to study on diet-induced fat accumulation and to evaluate effects of anti-obesity drugs using Drosophila. To understand overview of alterations of gene expression due to diet-induced fat accumulation and its suppression by the known anti-obesity drugs, we performed the RNA seq analyses. Consequently, mRNA levels of several genes involved in lipid metabolism, glycolysis/gluconeogenesis and anti-oxidative stress have changed in adults fed the HFD. Moreover, the levels altered in those fed on HFD supplemented with QG or EGCG. Our qRT-PCR further confirmed the RNA-seq data suggesting that expression of five genes essential for lipid metabolism was changed in HFD-fed animals and further altered in the animals treated with anti-obesity drugs. Among them, the most remarkable alteration was observed in dHSL gene encoding a lipase involved in lipid-storage after HFD feeding and the HFD supplemented with QG or EGCG. These changes are consistent with HFD-induced fat accumulation as well as the anti-obesity effects of those two drugs in mammals, suggesting that these genes play an important role in the anti-obesity effects of the drugs. These are the first evidences that whole profiles of altered gene expression under a condition of a diet-induced obesity and its suppression by anti-obesity drugs in Drosophila.
2018-10-20 | GSE121531 | GEO
Project description:Obesity is tightly associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms of obesity-induced fatty liver remain largely unknown.In order to identify genes that are potentially involved in dysfunctional hepatic lipid homeostasis in obesity, we performed a clustering analysis of Affymetrix arrays,which revealed that a number of mRNAs were dys-regulated in the livers of mice fed a high-fat diet (HFD), compared with mice fed a normal chow diet (ND).
2014-05-09 | GSE57425 | GEO
Project description:There is an increasing clinical evidence that obesity exerts deleterious effects on the skeleton. While obesity coexists with estrogen deficiency in postmenopausal women, their combined effects on the skeleton are poorly studied. Thus, we investigated the impact of high-fat diet (HFD) on bone and metabolism of ovariectomized (OVX) female mice (C57BL/6J). OVX or sham operated mice were fed either HFD (60%fat) or normal diet (ND) (10%fat) for 12 weeks. HFD-OVX group exhibited pronounced increase in body weight (~86% in HFD and ~122% in HFD-OVX, p<0.0005) and impaired glucose tolerance. Bone microCT-scanning revealed a pronounced decrease in trabecular bone volume/total volume (BV/TV) in HFD-OVX (15.6±0.48% in HFD and 37.5±0.235% in HFD-OVX, p<0.005) and expansion of bone marrow adipose tissue (BMAT) (+60.7±9.9% in HFD vs +79.5±5.86% in HFD-OVX, p<0.005). Mechanistically, HFD-OVX treatment led to upregulation of genes markers of senescence, bone resorption, adipogenesis and inflammation and downregulation of gene markers of bone formation and bone development. Similarly, HFD- OVX treatment resulted in significant changes in bone tissue levels of Purine/Pyrimidine and Glutamate metabolisms, known to play a regulatory role in bone metabolism. Obesity and estrogen deficiency exert combined deleterious effects on bone resulting in accelerated cellular senescence, expansion of BMAT and impaired bone formation leading to decreased bone mass. Our results suggest that obesity may increase bone fragility in post-menopausal women.
2022-12-05 | GSE194075 | GEO
Project description:Oxidative stress in adipose tissue and liver has been linked to the development of obesity. NADPH oxidases (NOX) enzymes are a major source of reactive oxygen species (ROS). The current study was designed to determine if NOX2-generated ROS play a role in development of obesity and metabolic syndrome after high fat feeding. Wild type (WT) mice and mice lacking the cytosolic NOX2 activated protein p47phox (P47KO) were fed AIN-93G diets or high fat diets (HFD) containing 45% fat and 0.5% cholesterol for 13 weeks from weaning. Affymetrix array analysis revealed dramatically less expression of mRNA of genes linked to energy metabolism, adipocyte differentiation (PPARM-NM-3, Runx2) and fatty acid uptake (CD36, lipoprotein lipase) in fat pads from female HFD-P47KO mice compared to HFD-WT females. These data suggest that NOX2 is an important regulator of metabolic homeostasis and that NOX2-associated ROS plays an important role in development of diet-induced obesity particularly in the female fat pads from p47phox and wild type fed a high fat or control diet
2012-11-01 | E-GEOD-41932 | biostudies-arrayexpress
Project description:Obesity is a leading cause of primary hypertension in children, and a high-fat intake and the gut microbiota may be involved in the pathogenesis of obesity-related hypertension (OrHTN), but the underlying mechanisms are not fully understood. Here, we show that high-fat diet (HFD) feeding alters the gut microbiota composition in OrHTN rats, resulting in a reduced abundance of the butyrate-producing bacteria Ruminococcus and a subsequent decrease in plasma butyrate levels. Histone 3 lysine 9 butyrylation (H3K9bu) levels decreased in the kidneys of OrHTN rats, which downregulates the expression of the hypertension-related MAS1 gene. Furthermore, sodium butyrate affected H3K9bu modification levels in a concentration-dependent manner, with decreased H3K9bu and downregulated MAS1 expression at low concentrations in human proximal tubular epithelial cells. Our results suggest that a HFD contributes to the development of OrHTN by altering the gut microbiota and its metabolites, leading to the downregulation of H3K9bu and hypertension-related gene expression.
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Project description:The objective of the experiment was to dissect the effects of a high-fat diet on juvenile adipose tissue gene expression under conditions of excess calorie intake versus normal calorie intake in comparison to a standard low-fat diet. For this purpose juvenile mice were fed (A) a standard low-fat diet (CD), (B) a high-fat diet ad libitum (excess calorie intake) (HFD) and (C) a high-fat diet with calorie consumption restricted to the calorie consumption of the CD diet (R-HFD). RNA expression was profiled after 1 week of feeding in the periuterine fat depot.
2019-04-09 | E-MTAB-7755 | biostudies-arrayexpress