Muscle unloading potentiates the effects of acetyl-L-carnitine on the slow oxidative muscle phenotype. (Articolo in rivista)

Type
Label
  • Muscle unloading potentiates the effects of acetyl-L-carnitine on the slow oxidative muscle phenotype. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Cassano P, Flück M, Giovanna Sciancalepore A, Pesce V, Calvani M, Hoppeler H, Cantatore P, Gadaleta MN. (2010)
    Muscle unloading potentiates the effects of acetyl-L-carnitine on the slow oxidative muscle phenotype.
    in BioFactors (Oxf.)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Cassano P, Flück M, Giovanna Sciancalepore A, Pesce V, Calvani M, Hoppeler H, Cantatore P, Gadaleta MN. (literal)
Pagina inizio
  • 70 (literal)
Pagina fine
  • 77 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 36 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Titolo
  • Muscle unloading potentiates the effects of acetyl-L-carnitine on the slow oxidative muscle phenotype. (literal)
Abstract
  • The effect of acetyl-L-carnitine (ALCAR) supplementation to 3-month-old rats in normal-loading and unloading conditions has been here investigated by a combined morphological, biochemical and transcriptional approach to test whether ALCAR might cause a remodeling of the metabolic/contractile phenotype of soleus muscle. Morphological assessment demonstrated an increase of type I oxidative fiber content and cross-sectional area in ALCAR-treated animals both in normal-loading and in unloading conditions. ALCAR prevented loss of mitochondrial mass in unloaded animals whereas no ALCAR-dependent increase of mitochondrial mass occurred in normal-loaded muscle. Validated microarray analysis delineated an ALCAR-induced maintenance of a slow-oxidative expression program only in unloaded soleus muscle. Indeed, the muscle adjustment of the expression profile of factors underlying mitochondrial oxidative metabolism, protein turnover, fiber type differentiation and an adaptation of voltage-gated ion channel expression was distinguishable with respect to the loading status. This selectivity may suggest a key role of muscle loading status in the manifestation of ALCAR effects. The results extend to a broader level of biological informations the previous notion on ALCAR positive effect in rat soleus muscle during unloading and point to a role of ALCAR for the maintenance of its slow-oxidative fiber character. (literal)
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