Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1217617 | ENA |
REPOSITORIES: ENA
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Project description:Aged (22-mo) female mice (n=35), obtained from the US NIH National Institute on Aging (NIA) Aged Rodent Colony, were randomly assigned to one of four groups: saline-treated sedentary ( n=9), nicotinamide N-methyltransferase inhibitor (NNMTi)-treated sedentary (10 mg/kg body weight; n=9), saline-treated progressive weighted wheel running (PoWeR; saline; n=10), and NNMTi-treated PoWeR (10 mg/kg body weight; n=7) . Group-housed Sed cohorts were compared to singly-housed PoWeR cohorts that underwent a 1-week introduction to an unweighted wheel, followed by eight weeks of weighted wheel running. Forelimb grip strength was assessed by a single NNMTi treatment-blinded investigator during week six and averaged across 2-4 trials/mouse. At the end of week 8, when mice were ~24.5-months-old, the strength of the right limb plantarflexor muscle complex was measured using an in vivo isometric peak tetanic torque technique and a fatigue test. After the fatigue test, mice were euthanized, and tissues were weighed and collected. Of note, hindlimb muscles from the right limb (the limb that underwent in vivo isometric peak tetanic torque and fatigue testing) were processed for immunohistochemistry to avoid acute effects of muscle functional testing on the proteome and metabolome. Hindlimb muscles from the left limb that did not undergo torque and fatigue testing were flash-frozen for proteome and metabolome analyses.
2024-05-07 | MSV000094700 | MassIVE
Project description:Androgens have a strong effect against skeletal muscles to increase muscle mass and strength. However, a molecular mechanism of AR action on muscle strength is not clear. To identify the target genes of AR in skeletal muscle, we generated myofiber specific ARKO using HSA-Cre and AR flox mice (cARKO). Nine-week-old female control and cARKO mice were treated with or without DHT for 4 weeks. After euthenization, gastrocunemius muscle were collected and total RNA were extracted.
2021-03-10 | GSE152756 | GEO
Project description:To test the hypothesis that different muscles may express variable amounts of different isoforms of muscle genes, we applied a custom-designed exon microarray containing probes for 57 muscle-specific genes to assay the transcriptional profiles in sets of human adult, lower limb skeletal muscles.
2015-06-17 | GSE69938 | GEO
Project description:As a consequence of impaired glucose or fatty acid metabolism, bioenergetic stress in skeletal muscles may trigger myopathy and rhabdomyolysis. Genetic mutations causing loss of function of the LPIN1 gene frequently lead to severe rhabdomyolysis bouts in children, though the metabolic alterations and possible therapeutic interventions remain elusive. Here, we show that lipin1 deficiency in mouse skeletal muscles is sufficient to trigger myopathy. Strikingly, muscle fibers display strong accumulation of both neutral and phospholipids. The metabolic lipid imbalance can be traced to an altered fatty acid synthesis and fatty acid oxidation, accompanied by a defect in acyl chain elongation and desaturation. As an underlying cause, we reveal a severe sarcoplasmic reticulum (SR) stress, leading to the activation of the lipogenic SREBP1c/SREBP2 factors, the accumulation of the Fgf21 cytokine, and alterations of SR-mitochondria morphology. Importantly, pharmacological treatments with the chaperone TUDCA and the fatty acid oxidation activator bezafibrate improve muscle histology and strength of lipin1 mutants. Our data reveal that SR stress and alterations in SR-mitochondria contacts are contributing factors and potential intervention targets of the myopathy associated with lipin1 deficiency.
2019-01-07 | MTBLS750 | MetaboLights
Project description:Microbiome research related to muscle strength improvement
| PRJEB85118 | ENA
Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
2024-12-31 | E-MTAB-14061 | biostudies-arrayexpress