Regulatory role of energy metabolism in skeletal development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA793909 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17417729.fastq.gz | Fastqsanger.gz | |||
| SRR17417730.fastq.gz | Fastqsanger.gz | |||
| SRR17417731.fastq.gz | Fastqsanger.gz | |||
| SRR17417732.fastq.gz | Fastqsanger.gz | |||
| SRR17417733.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:To test the consequence of reduced glycolysis and reduced cytoplasimic acetyl-CoA in mouse skeletal devleopment. To reduce glycolysis, Ldha was homozygously deleted in collagen 2 expressing chondrocytes using the Cre-lox sytem [Col2-Cre:Ldha(fl/fl)] on top of one allele germline deletion of Ldhb [Ldhb(+/-)]. To reduce cytoplasmic/nuclear acetyl-CoA, Acly that catalizes conversion of citreate into acetyl-CoA was deleted in chondrocytes using Col2-Cre. Both mutant mice develop skeletal dysplasia, but former model survive postnatally, whereas Acly mutants die at birth.
2022-04-01 | GSE192971 | GEO
Project description:Regulation and role of glycophagy in skeletal muscle energy metabolism
| PRJNA765027 | ENA
Project description:OTUD3 regulates energy metabolism
| PRJNA832095 | ENA
Project description:Functional and regulatory profiling of energy metabolism in fission yeast
| PRJEB12865 | ENA
Project description:Current atlas of regulatory sequences controlling skeletal muscle atrophy are still incomplete and lack cell type resolution. We applied single-cell chromatin accessibility assays (snATAC) to normal and denervated skeletal muscle from mice. We integrated these snATAC datasets with our single-nucleus RNA-sequence dataset to reveal the status of open chromatin. Using these datasets, we delineated chromatin accessibility maps in both normal and atrophic muscles and identified cis-regulatory elements (CREs) in all type of cell in skeletal muscle that may regulating muscle protein metabolism, energy metabolism and transcription activities, thus, provided a rich resource for understanding gene regulatory programs in skeletal muscle and related disorders.
2023-09-06 | GSE217575 | GEO
Project description:We aimed to investigate the human skeletal muscle (SkM) DNA methylome after exercise in low carbohydrate (CHO) energy balance (with high fat) compared with exercise in low-CHO energy deficit (with low fat) conditions. The objective to identify novel epigenetically regulated genes and pathways associated with ‘train-low sleep-low’ paradigms. The sleep-low conditions included 9 males that cycled to deplete muscle glycogen while reaching a set energy expenditure. Post-exercise, low-CHO meals (protein-matched) completely replaced (using high-fat) or only partially replaced (low-fat) the energy expended. The following morning resting baseline biopsies were taken and the participants then undertook 75 minutes of cycling exercise, with skeletal muscle biopsies collected 30 minutes and 3.5 hours post exercise. Discovery of genome-wide DNA methylation was undertaken using Illumina EPIC arrays and targeted gene expression analysis was conducted by RT-qPCR. At baseline participants under energy balance (high fat) demonstrated a predominantly hypermethylated (60%) profile across the genome compared to energy deficit-low fat conditions. However, post exercise performed in energy balance (with high fat) elicited a more prominent hypomethylation signature 30 minutes post-exercise in gene regulatory regions important for transcription (CpG islands within promoter regions) compared with exercise in energy deficit (with low fat) conditions. Such hypomethylation was enriched within pathways related to: IL6-JAK-STAT signalling, metabolic processes, p53 / cell cycle and oxidative / fatty acid metabolism. Hypomethylation within the promoter regions of genes: HDAC2, MECR, IGF2 and c13orf16 were associated with significant increases in gene expression in the post-exercise period in energy balance compared with energy deficit. Furthermore, histone deacetylase, HDAC11 was oppositely regulated at the gene expression level compared with HDAC2, where HDAC11 was hypomethylated yet increased in energy deficit compared with energy balance conditions. Overall, we identify some novel epigenetically regulated genes associated with train-low sleep-low paradigms.
2023-03-29 | GSE223786 | GEO
Project description:Obesity and physical inactivity have a profound impact on skeletal muscle metabolism. In the present work, we have investigated differences in protein expression and energy metabolism in primary human skeletal muscle cells established from lean donors (BMI<25 kg/m2) and individuals with obesity (BMI>30 kg/m2). Furthermore, we have studied the effect of fatty acid pretreatment on energy metabolism in myotubes from these donor groups. Alterations in protein expression were investigated using proteomic analysis, and energy metabolism was studied using radiolabeled substrates. Gene Ontology enrichment analysis showed that glycolytic, apoptotic, and hypoxia pathways were upregulated, whereas the pentose phosphate pathway was downregulated in myotubes from donors with obesity compared to myotubes from lean donors. Moreover, fatty acid, glucose, and amino acid uptake were increased in myotubes from individuals with obesity. However, fatty acid oxidation was reduced, glucose oxidation was increased in myotubes from subjects with obesity compared to cells from lean. Pretreatment of myotubes with palmitic acid (PA) or eicosapentaenoic acid (EPA) for 24 h increased glucose oxidation and oleic acid uptake. EPA pretreatment increased the glucose and fatty acid uptake and reduced leucine fractional oxidation in myotubes from donors with obesity. In conclusion, these results suggest that myotubes from individuals with obesity showed increased fatty acid, glucose, and amino acid uptake compared to cells from lean donors. Furthermore, myotubes from individuals with obesity had reduced fatty acid oxidative capacity, increased glucose oxidation, and a higher glycolytic reserve capacity compared to cells from lean donors. Fatty acid pretreatment enhances glucose metabolism, and EPA reduces oleic acid and leucine fractional oxidation in myotubes from donor with obesity, suggesting increased metabolic flexibility after EPA treatment
2023-03-11 | PXD037909 | Pride
Project description:We investigated the effect of weight loss maintenance (WLM) and weight regain on skeletal muscle in rodents. In skeletal muscle of obesity prone rats, WLM reduced fat oxidative capacity and down-regulated genes involved in fat metabolism. After weight was regained in rats, the genes involved in fat metabolism were still reduced. Mice with skeletal muscle lipoprotein lipase overexpression (mCK-hLPL), which augments fat metabolism, were subjected to our WLM and weight regain paradigm. We found that mCK-hLPL attenuated weight regain by potentiating energy expenditure.Irrespective of genotype, weight regain suppressed dietary fat oxidation and down-regulated genes involved in fat metabolism in skeletal muscle. However, mCK-hLPL mice oxidized more fat throughout weight regain and had greater expression of genes involved in fat metabolism and lower expression of genes involved in carbohydrate metabolism during WLM and regain.
2021-03-24 | GSE154943 | GEO
Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.
2019-08-01 | GSE130839 | GEO
Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.
2019-08-01 | GSE130838 | GEO