Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA143779 | ENA |
REPOSITORIES: ENA
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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:The effect of dietary calcium and dairy proteins on adipose tissue gene expression profile in diet induced obesity Experiment Overall Design: 9-week-old C57Bl/6J-mice were divided into two groups (n=10/group). The control diet was a standard high-fat diet (60% of energy) low in calcium (0.4%). The whey protein diet was a high-calcium (1.8%) high-fat diet with whey protein isolate. After the 21-week treatment, the adipose tissue transcript profiling (2 mice/group) was carried out using Affymetrix Mouse Genome 430 2.0 array.
2008-04-07 | E-GEOD-9280 | biostudies-arrayexpress
Project description:The purpose of this study is to investigate the role of SIRT1 in high-fat diet-induced liver steatosis and insulin resistance. SIRT1 is a nuclear enzyme that could remove an acetyl-group from target proteins by using NAD as co-substrate. Homologs of this protein in yeast and the roundworm C. elegans are able to delay the aging process in response to nutrients. However, the molecular mechanism by which SIRT1 sense the environment to mediate this response are poorly understood. We have shown that when chronically fed with a 40%-fat diet, SIRT1 heterozygous animals gain significantly more weight compared to wild type littermates. They are also hyperinsulimia, more insulin-resistant, and accumulate more lipids in liver. Interestingly, these animals also show signs of premature aging, such as an early appearance of gray fur, defective motor activity, and decreased fertility. In this microarray study, we analyzed the gene expression profiles in the liver of WT low-fat diet, Het low-fat diet, WT high-fat diet, and Het high-fat diet using Agilent Whole Genome Mouse 4x44 multiplex format oligo arrays following the Agilent-1-color microarray-based gene expression analysis protocol. This microarray analysis concluded that SIRT1 Het mice reponsed to the high-fat diet differently from the WT control mice. Liver total RNAs from SIRT1 WT and Het mice that were fed with either a low-fat diet or a high-fat diet for 34 weeks were used for a microarray gene expression study. Three biological replicates for each group were used.
2012-07-31 | E-GEOD-39778 | biostudies-arrayexpress
Project description:Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell–deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue–resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue–resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance. four samples
2012-08-06 | E-GEOD-39534 | biostudies-arrayexpress
Project description:Cockayne syndrome (CS) is an accelerated aging disorder characterized by progressive neurodegeneration caused by mutations in the genes encoding the DNA repair proteins CSA or CSB. Csbm/m mice were given a high-fat, caloric-restricted or resveratrol-supplemented diet. The high-fat diet rescued the phenotype of Csbm/m mice at the metabolic, transcriptomic and behavioral levels. Additional analysis suggests that the premature aging seen in CS mice, nematodes and human cells results from aberrant PARP activation due to deficient DNA repair leading to decreased SIRT1 activity and mitochondrial dysfunction. Notably, β-hydroxybutyrate levels are increased by the high-fat diet; and β-hydroxybutyrate, PARP inhibition, or NAD+ supplementation can activate SIRT1 and rescue CS-associated phenotypes. Mechanistically, CSB is able to displace activated PARP1 from damaged DNA to limit its activity. This study connects two emerging longevity metabolites, β-hydroxybutyrate and NAD+, through the deacetylase SIRT1 and suggests possible interventions for CS.
2014-12-22 | GSE62194 | GEO