Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA143779 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Adipose tissue plays an important role in storing excess nutrients and preventing ectopic lipid accumulation in other organs. Obesity leads to excess lipid storage in adipocytes, resulting in the generation of stress signals and the derangement of metabolic functions. SIRT1 is an important regulatory sensor of nutrient availability in many metabolic tissues. Here we report that SIRT1 functions in adipose tissue to protect from the development of inflammation and obesity under normal feeding conditions, and the progression to metabolic dysfunction under dietary stress. Genetic ablation of SIRT1 from adipose tissue leads to gene expression changes that highly overlap with changes induced by high fat diet in wild type mice, suggesting that dietary stress signals inhibit the activity of SIRT1. Indeed, we show that high fat diet induces the cleavage of SIRT1 in adipose tissue by the inflammation-activated caspase-1, providing a link between dietary stress and predisposition to metabolic dysfunction. Four replicates from four different biological conditions: 1) SIRT1 wild-type fed low fat diet, 2) SIRT1 wild-type fed high fat diet, 3) SIRT1 knock-out fed low fat diet, 4) SIRT1 knock-out fed high fat diet
2012-12-21 | E-GEOD-30247 | biostudies-arrayexpress
Project description:Adipose tissue plays an important role in storing excess nutrients and preventing ectopic lipid accumulation in other organs. Obesity leads to excess lipid storage in adipocytes, resulting in the generation of stress signals and the derangement of metabolic functions. SIRT1 is an important regulatory sensor of nutrient availability in many metabolic tissues. Here we report that SIRT1 functions in adipose tissue to protect from the development of inflammation and obesity under normal feeding conditions, and the progression to metabolic dysfunction under dietary stress. Genetic ablation of SIRT1 from adipose tissue leads to gene expression changes that highly overlap with changes induced by high fat diet in wild type mice, suggesting that dietary stress signals inhibit the activity of SIRT1. Indeed, we show that high fat diet induces the cleavage of SIRT1 in adipose tissue by the inflammation-activated caspase-1, providing a link between dietary stress and predisposition to metabolic dysfunction.
2012-12-21 | GSE30247 | GEO
Project description:Sirtuin1 (Sirt1) in skeletal muscle (SK) and fat protects against metabolic damage by stimulating insulin sensitivity. Here we report that mice with selective deletion of endothelial Sirt1 (E-Sirt1-KO) paradoxically exhibit heightened whole-body insulin sensitivity. Akt phosphorylation, glucose uptake, and glycolysis are boosted in SK and brown adipose tissue (BAT) of E-Sirt1-KO mice. E-Sirt1-KO mice have higher energy expenditure and are partially protected from high-fat diet-induced insulin resistance. Enhanced insulin sensitivity and peripheral tissue Akt phosphorylation in E-Sirt1-KO mice is transferrable to wild-type mice via the systemic circulation after surgical parabiosis. Silencing of Sirt1 in endothelial cells upregulates transcription of the F-actin-binding protein thymosin beta-4 (Tβ4), whose secretion activates Akt in skeletal myotubes. Sirt1 downregulation stimulates endothelial Tβ4 transcription through inhibition of autophagy and upregulation of nuclear factor-kappa B signaling. Thus, unlike Sirt1 in skeletal muscle and fat, endothelial Sirt1 curtails whole-body insulin sensitivity by inhibiting expression of secreted Tβ4.
2023-08-07 | PXD030565 | Pride
Project description:SIRT1 is a NAD+-dependent protein deacetylase. SIRT1 plays key roles in metabolic regulation and adaptation. In this study, we examined the difference of gene expression in brown adipose tissue from WT and SIRT1tg mice. SIRT1 transgenic model (heterozygous transgenic model) has already been described (Pfluger et al., 2008). Here we used homozygote transgenic mice which had been backcrossed to C57Bl/6N background. 3 months old WT and SIRT1tg mice were fed with a low fat diet. After sacrifice, total mRNA obtained from brown adipose were used for microarray.
2014-10-15 | E-GEOD-62324 | biostudies-arrayexpress
Project description:Adipose tissue remodeling is a dynamic process that involves adipocyte death and turnover. This study investigates the influence of miR-10a-5p on the remodeling of adipose tissue and the metabolic dysfunction prompted by a high-fat diet. Our objective involves examining the impact of a 16-week HFD feeding on both WT mice and miR-10a KO mice, comparing the genes that are differentially regulated based on the dietary intake.
2024-09-01 | GSE260771 | GEO
Project description:SIRT1 is a NAD+-dependent protein deacetylase. SIRT1 plays key roles in metabolic regulation and adaptation. In this study, we wanted to compare gene expression profile in SIRT1 overexpressing mice to WT mice submitted to different intervention (caloric restriction and exercise training) in different tissues (liver, skeletal muscle, brown and white adipose tissues). SIRT1 transgenic model has already been described (Pfluger et al., 2008). Here we used homozygote transgenic mice which had been backcrossed to C57Bl/6N background. 3 months old WT and SIRT1tg mice were fed with a low fat diet. After sacrifice, total mRNA obtained from brown adipose were used for microarray. Caloric restriction (CR) : everyother day feeding during 3 months Exercise training (EX) : mice were housed in running wheel cages during 10 weeks
2015-07-14 | E-GEOD-70857 | biostudies-arrayexpress
Project description:Metabolic disorders, such as obesity and type 2 diabetes, are major public health concerns worldwide. Dietary interventions, such as tea consumption, have been suggested as an effective strategy to prevent and treat metabolic disorders. White adipose tissue, as the main energy storage organ in mammals, plays a critical role in the regulation of whole-body metabolism. Recent studies have shown that the microenvironmental cell composition and metabolic network of white adipose tissue can be modulated by dietary factors, including tea consumption. However, the underlying mechanisms and the effects of tea consumption on white adipose tissue in the context of high-fat diet-induced metabolic disorders are not fully understood. Therefore, this study aimed to investigate the effects of tea consumption on the microenvironmental cell composition and metabolic network of white adipose tissue in high-fat diet-fed mice.
2023-12-11 | GSE235473 | GEO
Project description:Visceral white adipose tissue is closed correlated with obesity and metabolic dysfunction. Epididymal adipose tissue (eWAT) is considered as typical visceral white adipose tissue. Induction of browning of white adipose tissue improves metabolic dysfunction such as insulin resistance. In contrast to mice subcutaneous adipose tissue, visceral fat do not show significant browning under 4°C. However,under physiologically tolerable low temperature visceral adipose tissue can turn brown. We used microarrays to detail the global programme of gene expression in C57Bl/6 mice epididymal adipose tissue exposed to thermoneutral 30°C, 4°C and temperatures lower than 4°C.
2017-06-12 | GSE74062 | GEO
Project description:Maternal obesity is linked with increased adverse outcomes for mother and fetus. However, the metabolic impact of excessive fat accumulation within the altered hormonal context of pregnancy is not well understood. We used a murine model of obesity, the high fat diet-fed C57BL/6J mouse to determine adipose tissue-mediated molecular mechanisms driving metabolic dysfunction throughout pregnancy. Remarkably, obese mice exhibited a normalization of visceral fat accumulation at late-stage pregnancy (-53%, P<0.001 E18.5) to achieve levels comparable in mass (per gram of body weight) to that of non pregnant, control diet fed mice. Moreover, whilst obese pregnant mice showed a marked glucose intolerance and apparent insulin resistance at mid-stage pregnancy (E14.5), glucose homeostasis converged with that of lean pregnant mice at late-stage pregnancy, suggesting an unexpected amelioration of the worsening metabolic dysfunction in obese pregnant mice. Transcriptomic analysis of the late-stage visceral fat indicated reduced de novo lipogenic drive (Me1, Fasn, Scd1, Dgat2), retinol metabolism (Rdh11, Rbp4) and inflammation (Mcp1, Tnfα) in obese pregnant mice that was confirmed functionally by their lower adipose proinflammatory macrophage density. Elevated expression of estrogen receptor a (ERα) in visceral adipose tissue was identified as potential unifying mechanism for the transcriptional changes and reduced adiposity of late stage obese pregnancy. Support for a role for ERα was provided by experiments showing that the ERα selective agonist PPT suppressed lipogenesis in primary mouse adipocytes and suppressed Me1, Fasn, SCD1 and Dgat2 mRNA levels in mature female human ChubS7 clonal fat cells. Our data reveal a novel role for elevated visceral adipocyte estrogen signaling as a protective mechanism against visceral fat hypertrophy and inflammation in late pregnancy. Pregnant high fat, pregnant control fat, non pregnant high fat, non pregnant control fat. Five biologial replictes each (20 samples).
2013-12-31 | E-GEOD-48811 | biostudies-arrayexpress
Project description:White adipose tissue (WAT), once regarded as morphologically and functionally bland, is now recognized to be dynamic, plastic, heterogenous, and involved in a wide array of biological processes including energy homeostasis, glucose and lipid handling, blood pressure control, and host defense. High fat feeding and other metabolic stressors cause dramatic changes in adipose morphology, physiology, and cellular composition, and alterations in adiposity are associated with insulin resistance, dyslipidemia, and Type 2 diabetes (T2D). Here we provide detailed cellular atlases of human and murine subcutaneous and visceral white fat at single cell resolution across a range of body weight. We identify subpopulations of adipocytes, adipose stem and progenitor cells (ASPCs), vascular, and immune cells and demonstrate commonalities and differences across species and dietary conditions. We link specific cell types to increased risk of metabolic disease, and we provide an initial blueprint for a comprehensive set of interactions between individual cell types in the adipose niche in leanness and obesity. These data comprise an extensive resource for the exploration of genes, traits, and cell types in the function of WAT across species, depots, and nutritional conditions.
2022-01-11 | GSE176171 | GEO