Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse HFD Liver Skeletal Muscle SLC16A13 Knock-Out

ABSTRACT: Mouse HFD Liver Skeletal Muscle SLC16A13 Knock-Out

PROVIDER: PRJNA641022 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12066606.fastq.gz	Fastqsanger.gz
	SRR12066607.fastq.gz	Fastqsanger.gz
	SRR12066608.fastq.gz	Fastqsanger.gz
	SRR12066609.fastq.gz	Fastqsanger.gz
	SRR12066610.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 44

Similar Datasets

Skeletal muscle cystathionine γ-lyase deficiency promotes obesity and insulin resistance and results in hyperglycemia and skeletal muscle injury upon HFD in mice

Project description:In the present study, we explored whether skeletal muscle cystathionine γ-lyase (CTH) contributes to high-fat diet (HFD)-induced metabolic disorders using skeletal muscle Cth knockout (CthΔskm) mice. Metabolomics coupled with transcriptome showed that CthΔskm mice displayed impaired energy metabolism and some signaling pathways linked to insulin resistance (IR) in skeletal muscle although the mice had normal insulin sensitivity. HFD led to reduced CTH expression and impaired energy metabolism in skeletal muscle in Cth-floxed mice (Cthf/f) mice. CTH deficiency and HFD had some common pathways enriched in the aspects of amino acid metabolism, carbon metabolism, and fatty acid metabolism. CthΔskm+HFD mice exhibited increased body weight gain, fasting blood glucose, plasma insulin, and IR, and reduced glucose transporter 4 and CD36 expression in skeletal muscle compared to Cthf/f+HFD mice. Impaired mitochondria and irregular arrangement in myofilament occurred in CthΔskm+HFD mice. Omics analysis showed differential pathways enriched between CthΔskm mice and Cthf/f mice upon HFD. More severity in impaired energy metabolism, reduced AMPK signaling, and increased oxidative stress and ferroptosis occurred in CthΔskm+HFD mice compared to Cthf/f+HFD mice. Our data indicate that skeletal muscle CTH expression dysregulation contributes to metabolism disorders upon HFD.

2024-05-11 | GSE254704 | GEO

Skeletal muscle gene expression in the wild type and the GAA knock-out mice, a model of Pompe disease

Project description:Pompe disease is a Lysosomal glycogen storage disorder due to the deficiency of acid alpha glucosidase. The enzyme degrades glycogen to glucose and its deficiency results in progressive enlargement of glycogen-filled lysosomes in multiple tissues with skeletal and cardiac muscle most severely affected clinically. Clinical spectrum ranges from most severe infantile cardiomegally and skeletal muscle myopathy to milder late onset forms with only skeletal muscle pathology. The currently available enzyme replacement therapy has only limited effect in skeletal muscle. Here we use RNA sequencing of therapy-resistant skeletal muscle (white part of gastrocnemius muscle) to identify the differencies between the diseased and healthy muscle. Total RNA was obtained from gastrocnemius muscle (white part) of acid alpha glucosidase knock-out and wild-type mice.

2017-05-13 | E-GEOD-57980 | biostudies-arrayexpress

Gene expression in skeletal muscle in AMPK gamma3 knock-out mice and wild type littermates

Project description:Analysis of AMPK gamma3-dependent transcriptional responses by analyzing global gene expression in the white portion of the gastrocnemius muscle in AMPK gamma3 knock-out mice and corresponding wild type littermates. Keywords: Genetic modification

2006-02-15 | GSE4063 | GEO

Muscle Clock knock out mice metabolic changes (iMSBmal1-Exp1)

Project description:My lab studies the function of the molecular clocks in skeletal muscle. We have an inducible genetic mouse model (C57Bl6 background) in which we knock out the core clock gene, Bmal1, only in adult skeletal muscle after treatment with tamoxifen. We have found that the mice maintain body mass but lose fat mass at 10 weeks after loss of Bmal1. We have done expression profiling on the skeletal muscles and gene expression changes (insulin signaling, CHO metabolism, fat metabolism) suggest significant changes in substrate metabolism. To analyze TCA, CHO metabolites we have collected gastrocnemius muscles from these mice following instructions from Dr. Burant. Mice were anaesthetized with isoflurane, the gastrocnemius muscle dissected and flash frozen with tongs cooled with liquid N2. They have been stored in cryovials in our -80 freezer for 2 months.

2015-03-26 | ST000313 | MetabolomicsWorkbench

Gene expression changes in Jhdm2a knock-out skeletal muscle as compared to wild-type.

Project description:Gene expression changes in mouse skeletal muscle were assessed in wild-type and Jhdm2a null skeletal muscle in an effort to define the role of Jhdm2a in energy expenditure and metabolism.

2009-02-05 | GSE13552 | GEO

Mouse HFD Liver Skeletal Muscle SLC16A13 Knock-Out

Project description:Genome-wide association identified SLC16A13 as novel type 2 diabetes gene locus. The SLC16A13 gene encodes for SLC16A13/MCT13, member of the solute carrier 16 family of monocarboxylate transporters. This transporter family recently raised interest in metabolic research with the identification of SLC16A11 polymorphisms associated with type 2 diabetes; and human as well as mouse data suggest causal relationship between SLC16A11/MCT11 transporter dysfunction and type 2 diabetes development. In contrast, SLC16A13 biology and physiological function is not characterized at all. Here, we validate SLC16A13 as monocarboxylate transporter expressed at the plasma membrane and report the first Slc16a13 knockout mouse line. Deletion of Slc16a13 ameliorates metabolic disease in the context of diet-induced obesity. The improved metabolic phenotype is characterized by increased mitochondrial respiration in the liver, leading to reduced hepatic lipid accumulation and increased insulin sensitivity of Slc16a13 knockout mice. Mechanistically, we propose reduced intracellular lactate availability in Slc16a13 knockout hepatocytes, affecting hepatic energy metabolism by AMPK activation and increased oxidative phosphorylation, reducing hepatic lipid content and insulin resistance in obese mice. Together, these data suggest SLC16A13/MCT13 as potential novel target to treat fatty liver, insulin resistance and related metabolic disorders.

2021-06-24 | GSE152937 | GEO

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

Transcriptomic profile of skeletal muscle in wild-type, GAA knock-out, and AAV treated GAA knock-out mice to understand Pompe disease mechanisms and assess therapeutic efficacy

Project description:Transcriptomic profile of skeletal muscle in wild-type, GAA knock-out, and AAV treated GAA knock-out mice to understand Pompe disease mechanisms and assess therapeutic efficacy

| PRJNA667501 | ENA

Changes in skeletal muscle PAK1 levels regulate tissue crosstalk to impact whole body glucose homeostasis

Project description:We have used RNA-seq to identify transcripts expressed in mouse skeletal muscle inducible PAK1 overexpression/knock-out.

2022-02-08 | GSE191000 | GEO

Transcription profiling of mouse skeletal muscle of AMP-activated protein kinase gamma3 R225Q transgenic versus knock-out

2007-12-14 | E-GEOD-4063 | biostudies-arrayexpress