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Dietary fish oil alleviates soleus atrophy during immobilization in association with Akt signaling to p70s6k and E3 ubiquitin ligases in rats.
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- Author(s): Jae-Sung You; Mi-Na Park; Wook Song; Yeon-Sook Lee
- Source:
Applied Physiology, Nutrition & Metabolism; Jun2010, Vol. 35 Issue 3, p310-318, 8p, 2 Charts, 5 Graphs- Subject Terms:
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- Abstract: Reduced muscle activity leads to impaired insulin signaling, which leads to loss of contractile proteins and muscle mass via the Akt pathway. Dietary fish oil rich in long chain n-3 polyunsaturated fatty acids has been shown to prevent insulin signaling resistance in skeletal muscle. This study was conducted to elucidate the protective effect of dietary fish oil on disuse-induced perturbations in insulin signaling and soleus muscle atrophy. To accomplish this, rats were fed a corn-oil- (control) or fish-oil-based diet for 2 weeks, and then subjected to hindlimb immobilization while still receiving the same diets. After 10 days of immobilization, the soleus muscle mass and myosin heavy chain level had markedly decreased; however, these losses were significantly suppressed in rats fed dietary fish oil, compared with the control group. Dietary fish oil nearly completely attenuated the disturbances in activation of the Akt and p70 S6 kinase proteins, as well as the gene expression of muscle-specific E3 ubiquitin ligases (muscle atrophy F-box and muscle RING finger 1). However, insulin receptor substrate 1 associated with the p85 subunit of phosphoinositide 3-kinase was not altered during immobilization. Dietary fish oil also inhibited alterations in the gene expression of cyclooxygenase-2 and inducible nitric oxide synthase, with no additional observation of oxidative stress. Collectively, these findings indicate that dietary fish oil prior to and during immobilization may alleviate the immobilization-induced soleus muscle atrophy, at least in part, via the Akt pathway through E3 ubiquitin ligases and p70s6k. La diminution de l’activité musculaire aboutit à des anomalies de signalisation de l’insuline dans la voie de l’Akt, entraînant ainsi la perte de protéines contractiles et de masse musculaire. L’huile de poisson riche en acides gras n-3 polyinsaturés à longue chaîne prévient, selon des données probantes, la signalisation de l’insulinorésistance dans le muscle squelettique. Cette étude a pour objet d’évaluer l’effet protecteur de l’huile de poisson ajoutée au régime sur les perturbations de la signalisation de l’insuline suscitées par l’inaction et sur l’atrophie du muscle soléaire. À cette fin, on donne à des rats de l’huile de maïs (contrôle) ou de l’huile de poisson durant 2 semaines, puis on immobilise leurs pattes arrière tout en continuant le même régime alimentaire. Après 10 jours d’immobilisation, la masse musculaire du soléaire et la concentration de la myosine à chaîne lourde diminuent, mais ces pertes sont contrées significativement chez les rats alimentés en huile de poisson, comparativement aux rats du groupe de contrôle. L’huile de poisson ajoutée aux aliments atténue presque complètement les problèmes d’activation de l’Akt et de la p70 S6-kinase et l’expression génique des E-3 ubiquitine ligases (MAF-bx et murf 1). Par contre, le substrat du récepteur de l’insuline associé à la sous-unité p85 de la phosphoinositide 3-kinase n’est pas modifié par l’immobilisation. L’huile de poisson ajoutée aux aliments inhibe aussi les altérations de l’expression génique de la cyclooxygénase-2 et la forme inductible de l’oxyde nitrique synthase, et ce, sans la manifestation de stress oxydatif. Globalement, ces observations révèlent que la consommation d’huile de poisson avant et durant l’immobilisation atténue l’atrophie du muscle soléaire au moyen des E3 ubiquitine ligases et de la p70 S6 kinase dans la voie de l’Akt. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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