Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nucleosome maps in skeletal muscle in response to diet in vivo

ABSTRACT: The nucleosome signature reflects the cellular epigenetic memory and contributes to the cellular phenotype and function. Obesity and type 2 diabetes pathogenesis is largely dependent on environmentally-induced epigenetic modifications and is marked by skeletal muscle insulin resistance; however, no in vivo skeletal muscle nucleosome maps exist to date. Herein, whole genome nucleosome maps via MNase-seq in skeletal muscle of mice on a low fat, high fat or high fat diet with the chromatin modifier sodium butyrate show that complex interactions among mitochondrial function, the tissue microenvironment, cellular phenotype and nucleosome landscape determine whole body phenotype and insulin resistance.

ORGANISM(S): Mus musculus

PROVIDER: GSE37913 | GEO | 2012/05/11

SECONDARY ACCESSION(S): PRJNA165665

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nucleosome maps in skeletal muscle in response to diet in vivo

Project description:The nucleosome signature reflects the cellular epigenetic memory and contributes to the cellular phenotype and function. Obesity and type 2 diabetes pathogenesis is largely dependent on environmentally-induced epigenetic modifications and is marked by skeletal muscle insulin resistance; however, no in vivo skeletal muscle nucleosome maps exist to date. Herein, whole genome nucleosome maps via MNase-seq in skeletal muscle of mice on a low fat, high fat or high fat diet with the chromatin modifier sodium butyrate show that complex interactions among mitochondrial function, the tissue microenvironment, cellular phenotype and nucleosome landscape determine whole body phenotype and insulin resistance. Skeletal muscle samples (n=5 per group) were pooled after homogenization under liquid nitrogen with a motar and pestle to give one sample per group for MNase-seq

2012-05-11 | E-GEOD-37913 | biostudies-arrayexpress

MicroRNA signature in skeletal muscle in insulin resistant rats

Project description:The current study aimed to address the hypothesis that programmed expression of key miRNAs in skeletal muscle mediates the development of insulin resistance, and consequently long-term health. We thus examined microRNA signatures in skeletal muscle of programmed insulin resistant rats offspring from high fat-fed dams vs control offspring from chow fed dams. Skeletal muscle (soleus) was collected from the hind limb of 1 year old male offspring (6 from control dams, 6 from high fat-fed dams) . Ramaciotti Centre for Genomics (UNSW, sydney, Australia)

2015-04-25 | E-GEOD-68225 | biostudies-arrayexpress

Proteomics analysis of white adipose tissue in high fat diet fed mice

Project description:The popularity of high fat foods in modern society has been associated with epidemic of various metabolic diseases characterized by insulin resistance, the pathology of which involves complex interactions between multiple tissues such as liver, skeletal muscle and white adipose tissue (WAT). To uncover the mechanism by which excessive fat impairs insulin sensitivity, we conducted a multi- tissue study by using TMT-based quantitative proteomics. 3-week-old ICR mice were fed with high fat diet (HFD) for 19 weeks to induce insulin resistance. Liver, skeletal muscle and epididymal fat were collected for proteomics screening. Additionally, PRM was used for validating adipose differential proteins. By comparing tissue-specific protein profiles of HFD mice, multi-tissue regulation of glucose and lipid homeostasis and corresponding underlying mechanisms was systematically investigated and characterized.

2022-04-04 | PXD021019 | Pride

The effects of serotonin by Tph1 and Htr2b on skeletal muscle

Project description:It is known that reducing circulating serotonin by inhibiting Tph1 increases the sensitivity of BAT cells and this drives thermogenesis by fat and glucose oxidation. In our results inhibiting Tph1 in muscle showed activation of SIRT1/LKB1/AMPK pathway in skeletal muscle cells and increased p-ACC. Also, it's known that inhibiting adipose Htr2b signaling ameliorates HFD-induced systemic insulin resistance. Here we report insulin sensitivity changes by regulating serotonin in skeletal muscle by Htr2b. Inhibiting Htr2b increases AMPK activity, glucose uptake, and myofiber size and decreases lipid droplet accumulation in HFD mice skeletal muscle. These results indicate improved insulin resistance and myosteatosis in skeletal muscle by lack of Serotonin by Tph1/Htr2b on skeletal muscle.

2024-08-29 | GSE275857 | GEO

Proteomics analysis of insulin sensitive tissues in high fat diet fed mice

2022-01-26 | PXD021046 | Pride

MicroRNA signature in skeletal muscle in insulin resistant rats

2015-04-25 | GSE68225 | GEO

Effect of myostatin inhibition on skeletal muscle gene expression in high fat diet-fed mice

Project description:Myostatin (GDF8) is a member of the TGF-beta family of proteins which is predominantly expressed in skeletal muscle and acts as a negative regulator of muscle mass. Inhibition of myostatin leads to muscle hypertrophy and has been shown to mitigate insulin resistance in mouse models of type 2 diabetes, although the mechanisms underlying this effect are unclear. We found that myostatin inhibition by AAV-mediated overexpression of the myostatin propeptide improves skeletal muscle insulin sensitivity in mice made insulin-resistant by high fat diet feeding. To gain insight into potential gene expression changes responsible for this effect, we performed microarray analysis on skeletal muscle samples from high fat diet-fed mice with and without myostatin inhibition.

2020-05-29 | GSE130622 | GEO

Changes in endothelial cell secretome after sirtuin-1 knock-down

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

The effects of serotonin by Tph1 on skeletal muscle

Project description:Reducing circulating serotonin by inhibition of Tph1 increases the sensitivity of BAT cells and this drives thermogenesis by fat and glucose oxidation. Here we report Insulin sensitivity changes by regulating Serotonin on skeletal muscle. Improved glucose tolerance and insulin sensitivity in HFD Tph1 KO mice. Inhibiting Tph1 increases AMPK activity, glucose uptake, myofiber size and decreases lipid droplet accumulation in HFD mice skeletal muscle. Inhibiting Tph1 in muscle showed activation of SIRT1/LKB1/AMPK pathway in skeletal muscle cells and increased p-ACC. Theses results indicates that protected insulin resistance and myosteatosis on skeletal muscle by lack of Serotonin by Tph1 on skeletal muscle.

2024-10-17 | GSE279210 | GEO

Muscle Specific Insulin Receptor Overexpression Protects Mice from Diet-Induced Glucose Intolerance but Leads to Post-Receptor Insulin Resistance

Project description:Skeletal muscle insulin resistance is a prominent early feature in the pathogenesis of type 2 diabetes (T2D). In attempt to overcome this defect, we generated mice overexpressing insulin receptors (IR) specifically in skeletal muscle (IRMOE). On normal chow, IRMOE mice have similar body weight as controls, but an increase in lean mass and glycolytic muscle fibers and reduced fat mass. IRMOE mice also show higher basal phosphorylation of IR, IRS-1 and Akt in muscle and improved glucose tolerance compared to controls. When challenged with high fat diet (HFD), IRMOE mice are protected from diet-induced obesity. This is associated with reduced inflammation in fat and liver, improved glucose tolerance and improved systemic insulin sensitivity. Surprisingly, however, in both chow and HFD-fed mice, insulin stimulated Akt phosphorylation is significantly reduced in muscle of IRMOE mice, indicating post-receptor insulin resistance. RNA sequencing reveals downregulation of several post-receptor signaling proteins that contribute to this resistance. Thus, enhancing early insulin signaling in muscle by overexpression of the insulin receptor protects mice from diet-induced obesity and its effects on glucose metabolism. However, chronic overstimulation of this pathway leads to post-receptor desensitization, indicating the critical balance between normal signaling and hyperstimulation of the insulin signaling pathway.

2020-09-01 | GSE149662 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data