Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass II

ABSTRACT: Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass II

PROVIDER: PRJNA1049427 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27113525_1.fastq.gz	Fastqsanger.gz
	SRR27113525_2.fastq.gz	Fastqsanger.gz
	SRR27113526_1.fastq.gz	Fastqsanger.gz
	SRR27113526_2.fastq.gz	Fastqsanger.gz
	SRR27113527_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 68

Similar Datasets

Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass II

Project description:We propose that the Muscle-Brain-Gut axis regulates skeletal muscle mass through the defined mechanism.

2023-12-13 | GSE249515 | GEO

Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass

Project description:We propose that the Muscle-Brain-Gut axis regulates skeletal muscle mass through the defined mechanism.

2023-12-11 | GSE249324 | GEO

Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass

Project description:Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass

| PRJNA1048525 | ENA

Effect of an Oral Nutritional Supplement on Muscle Mass During Anticancer Treatment

Project description:Malnutrition and low muscle mass (sarcopenia) are common problems in patients with cancer. However, a low muscle mass is associated with negative clinical outcomes in patients with cancer. Therefore, it is very important to maintain muscle mass in this population. This study aims to investigate the effect of an oral nutritional supplement on skeletal muscle mass during anti-cancer treatment.

| 2256 | ecrin-mdr-crc

FBXW7 coordinates postprandial muscle glucose metabolism and maintenance of skeletal muscle mass

Project description:In this study, we show that muscle-specific inactivation of FBXW7 elicits striking defects in postprandial glucose metabolism and failure to maintain skeletal muscle mass in adult mice. Further, mice lacking FBXW7 exhibited impaired endurance capacity and exacerbated HFD-induced insulin resistance and postprandial hyperglycemia. At the mechanistic level, RNAseq and quantitative proteomic analysis revealed global effects of FBXW7 deficiency on skeletal muscle transcriptome and proteome. This work illustrates a prominent role of FBXW7 in integrating postprandial nutritional signals to coordinate glucose metabolism and muscle mass maintenance.

2024-06-21 | GSE140503 | GEO

Succinate dehydrogenase (SDH)-Complex II regulates skeletal muscle cellular respiration and fatigue but not muscle mass in genetically induced pulmonary emphysema [20 wk]

Project description:Skeletal muscle wasting and reduced oxidative capacity coexist in patients with COPD/pulmonary emphysema and are independently associated with higher mortality. Whether reduced respiration contributes to muscle atrophy in that setting remains unknown. We have previously shown that a mouse with genetically induced COPD/pulmonary emphysema recapitulates muscle dysfunction features present in patients’ muscles, including reduced expression and activity of succinate dehydrogenase (SDH), which are partially reversed by genetic gain of SDH function. Previous research suggests that succinate accumulation, a by-product of SDH inhibition, can increase respiratory capacity of skeletal muscle. Here, we generated an inducible, muscle-specific SDH-C knockout mouse which demonstrates lower mitochondrial oxygen consumption and oxidative fibers’ contractility, associated with overall reduced exercise endurance. These changes are partially offset by mitochondrial complex I-dependent respiration, a respiratory pattern replicated in the muscles from the COPD/pulmonary emphysema genetic model. Moreover, while mice skeletal muscle SDH-C knockout causes an early succinate accumulation associated with a downregulated transcriptome, these changes do not correlate with the proteomic landscape; and animals muscle mass, fiber-type composition, and dry body mass constituents remain unaltered. We preset the first conditional, skeletal muscle-specific SDH-C knockout animal and demonstrate that while SDH-C regulates fibers respiration in genetically induced pulmonary emphysema, it does not control muscle mass.

2024-02-24 | GSE255635 | GEO

Succinate dehydrogenase (SDH)-Complex II regulates skeletal muscle cellular respiration and fatigue but not muscle mass in genetically induced pulmonary emphysema [3 wk]

2024-02-24 | GSE255632 | GEO

FBXW7 coordinates postprandial muscle glucose metabolism and maintenance of skeletal muscle mass

Project description:FBXW7 coordinates postprandial muscle glucose metabolism and maintenance of skeletal muscle mass

| PRJNA589977 | ENA

Estrogen receptor β regulates skeletal muscle mass and muscle stem cell proliferation in young female mice

Project description:The female sex hormone estrogens plays a critical role in maintaining muscle mass and muscle stem cell (MuSCs) functions. However, it is still unclear about downstream pathways of estrogens including its receptors that are expressed in both skeletal muscle tissue and MuSCs. To study the specific role of estrogen receptor β (ERβ), one of two main types of estrogen receptors, in skeletal muscle and MuSCs, we generated muscle-specific ERβ-knockout (mKO) mice and muscle stem cell-specific ERβ-knockout (scKO) mice. Here, we show that muscle-specific ERβ-deficient induced decreased muscle strength and fast-type muscle mass in young female mice. Furthermore, muscle stem cell-specific ERβ-deficient young female mice but not male exhibited impaired muscle regeneration ability after acute muscle injury, accompanied by a decreased proliferation rate of muscle stem cells. RNA sequencing analysis showed that the loss of ERβ in muscle stem cells changes the expression of cell cycle associated genes and niche component factors including laminin and collagen. Thus, our characterization of mKO and scKO mice indicate that the estrogen-ERβ pathway is a sex-specific regulatory mechanism that controls both skeletal muscle mass and the proliferation of muscle stem cell in females and could be of importance in a therapeutic context.

2020-03-31 | GSE135837 | GEO

The Mitochondrial Calcium Uniporter controls skeletal muscle mass in vivo

Project description:Muscle atrophy contributes to the poor prognosis of many physiopathological conditions, but pharmacological therapies are still limited. Muscle activity leads to major swings in mitochondrial [Ca2+] which control aerobic metabolism, cell death and survival pathways. We have investigated in vivo the effects of mitochondrial Ca2+ homeostasis in skeletal muscle function and trophism, by overexpressing or silencing the Mitochondrial Calcium Uniporter (MCU). The results coherently demonstrate that both in developing and in adult muscles MCU-dependent mitochondrial Ca2+ uptake has a marked trophic effect that does not depend on autophagy or aerobic control, but impinges on two major hypertrophic pathways of skeletal muscle, PGC-1M-NM-14 and Igf1-Akt/PKB. In adult mice, MCU overexpression protects from denervation-induced atrophy. These data reveal a novel Ca2+-dependent organelle-to-nucleus signaling route, which links mitochondrial function to the control of muscle mass and may represent a possible pharmacological target in sarcopenia. Experiments were performed on biological replicates of single skeletal muscle fibres. Seven fibres were chosen for their Mutochondrial Calcium Uniporter (MCU) overexpression and other seven fibres because MCU was silenced. Overexpression and silencing were performed injecting skeletal muscle with AAV containing MCU gene or short interfering oligos specific for MCU. As control was profiled eigth fibres transfected with AAV and eigth wild type fibres. Analyses were performed 7 days and 14 days after the AAV injection (3 fibers after 7 days and 4 fibers after 14 days for MCU overexpression and silencing, four fibres after 7 days and four after 14 days for control).

2015-03-05 | E-GEOD-60931 | biostudies-arrayexpress

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