Glucose deprivation promotes activation of mTOR signaling pathway and protein synthesis in rat skeletal muscle cells.
Pflugers Arch
; 467(6): 1357-66, 2015 Jun.
Article
en En
| MEDLINE
| ID: mdl-25074488
ABSTRACT
Signaling through mammalian target of rapamycin (mTOR) has been shown to play a central role in the regulation of skeletal muscle growth induced by a wide range of stimuli either mechanical or metabolic, such as growth factors and amino acids. Here, we demonstrate that mTOR and its downstream target, the ribosomal S6 kinase (p70(S6K)), are activated in L6 myocytes by a short-term glucose deprivation. Such response is specific of skeletal muscle and is likely responsible for the increased rate of protein synthesis and expression of the muscle-specific proteins during recovery from glucose deprivation. Nitric oxide and phosphatidylinositol-3-kinase (PI3K) are upstream positive regulators of mTOR since their pharmacological inhibition prevents the activation of p70(S6K) in response to glucose deprivation. We therefore propose a model of response to a brief period of glucose deprivation that may occur in skeletal muscle cells during resistance exercise and that may lead to protein accretion when blood flow recovers and all nutrients are again available.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Biosíntesis de Proteínas
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Transducción de Señal
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Mioblastos Esqueléticos
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Serina-Treonina Quinasas TOR
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Glucosa
Tipo de estudio:
Prognostic_studies
Límite:
Animals
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Humans
Idioma:
En
Año:
2015
Tipo del documento:
Article