ArticleSkeletal muscle2016
Alterations to mTORC1 signaling in the skeletal muscle differentially affect whole-body metabolism.
Article in Skeletal muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Constitutive mTORC1 activation in skeletal muscle increases inflammation but is not sufficient to impair glucose tolerance.Function (Oxford, England) · 2026Article
- Regulation of survival, growth, and metabolism by neuronal mTOR.GeroScience · 2026Article
- Equation-derived SMI not generalizable for DXA-defined low muscle mass in Chinese adults: external validation study.Frontiers in nutrition · 2026Article
- AKT-mediated phosphorylation of TSC2 controls stimulus- and tissue-specific mTORC1 signaling and organ growth.Developmental cell · 2025Article
- mTORC1 in energy expenditure: consequences for obesity.Nature reviews. Endocrinology · 2024Review
- Elevated BCAA catabolism reverses the effect of branched-chain ketoacids on glucose transport in mTORC1-dependent manner in L6 myotubes.Journal of nutritional science · 2024Article
- Geroprotector drugs and exercise: friends or foes on healthy longevity?BMC biology · 2023Review
- Metabolomic and Lipidomic Signature of Skeletal Muscle with Constitutively Active Mechanistic Target of Rapamycin Complex 1.The Journal of nutrition · 2023Article
- Review
- Regulation and metabolic functions of mTORC1 and mTORC2.Physiological reviews · 2021Review
- Deletion ofJBMR plus · 2021Article
- The mTORC1 complex in pre-osteoblasts regulates whole-body energy metabolism independently of osteocalcin.Bone research · 2021Article
- Edward F. Adolph Distinguished Lecture. Skeletal muscle atrophy: Multiple pathways leading to a common outcome.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
- A novel voluntary weightlifting model in mice promotes muscle adaptation and insulin sensitivity with simultaneous enhancement of autophagy and mTOR pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Enhanced skeletal muscle insulin sensitivity after acute resistance-type exercise is upregulated by rapamycin-sensitive mTOR complex 1 inhibition.Scientific reports · 2020Article
- RNA-sequencing analysis reveals the potential contribution of lncRNAs in palmitic acid-induced insulin resistance of skeletal muscle cells.Bioscience reports · 2020Article
- Ketones for Post-exercise Recovery: Potential Applications and Mechanisms.Frontiers in physiology · 2020Review
- Skeletal muscle-specific knockout of DEP domain containing 5 protein increases mTORC1 signaling, muscle cell hypertrophy, and mitochondrial respiration.The Journal of biological chemistry · 2019Article
- Lack of muscle mTOR kinase activity causes early onset myopathy and compromises whole-body homeostasis.Journal of cachexia, sarcopenia and muscle · 2019Article
- Role of mTOR in Glucose and Lipid Metabolism.International journal of molecular sciences · 2018Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mammalian target of rapamycin complex 1 (mTORC1) is a central node in a network of signaling pathways controlling cell growth and survival. This multiprotein complex integrates external signals and affects different nutrient pathways in various organs. However, it is not clear how alterations of mTORC1 signaling in skeletal muscle affect whole-body metabolism.
resultsWe characterized the metabolic phenotype of young and old raptor muscle knock-out (RAmKO) and TSC1 muscle knock-out (TSCmKO) mice, where mTORC1 activity in skeletal muscle is inhibited or constitutively activated, respectively. Ten-week-old RAmKO mice are lean and insulin resistant with increased energy expenditure, and they are resistant to a high-fat diet (HFD). This correlates with an increased expression of histone deacetylases (HDACs) and a downregulation of genes involved in glucose and fatty acid metabolism. Ten-week-old TSCmKO mice are also lean, glucose intolerant with a decreased activation of protein kinase B (Akt/PKB) targets that regulate glucose transporters in the muscle. The mice are resistant to a HFD and show reduced accumulation of glycogen and lipids in the liver. Both mouse models suffer from a myopathy with age, with reduced fat and lean mass, and both RAmKO and TSCmKO mice develop insulin resistance and increased intramyocellular lipid content.
conclusionsOur study shows that alterations of mTORC1 signaling in the skeletal muscle differentially affect whole-body metabolism. While both inhibition and constitutive activation of mTORC1 induce leanness and resistance to obesity, changes in the metabolism of muscle and peripheral organs are distinct. These results indicate that a balanced mTORC1 signaling in the muscle is required for proper metabolic homeostasis.
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