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Le métabolisme lipidique dans les altérations mitochondriales induites par l’absence de myostatine : impact de l’entrainement en endurance

Abstract : Myostatin (mstn) inactivation or inhibition is considered as a promising treatment for various muscle-wasting disorders because it promotes muscle growth. However, mstn-deficient hypertrophic muscles show strong fatigability associated with abnormal mitochondria and lipid metabolism. Muscle membrane maintains the structure and the metabolic function of the fibre, and mitochondrial membrane including respiratory chain complexes, are composed mainly of lipids and phospholipids playing functional role in mitochondrial bioenergetics. In our study, we hypothesized first that changes in the muscle and mitochondrial lipid composition could exist in the KO mstn muscle, in relation with the metabolic and functional alterations, secondly that endurance training can normalize these phenotypic muscle alterations. We reported in KO mstn muscles a decrease of fat membrane transporter levels (FAT/CD36, FABP3, FATP1 and FATP4) associated with decreased lipid oxidative pathway (citrate synthase and βHAD activities) and decreased lipogenesis (decreased triglyceride and free fatty acids content). Interestingly, we demonstrated a decrease in mitochondrial cardiolipin content, in relation with a decrease in PGPS and CRLS1 gene expressions. Then, we showed in KO mstn mice that 4 weeks of daily running exercise session (65-70% of the maximal aerobic speed for 1 hour) improved significantly aerobic performance, particularly the endurance to levels comparable to those of trained wild type littermates.The expression of oxidative and lipid metabolism markers also was increased, as indicated by the upregulation of the Cpt1, Ppar, Fas genes, and increased citrate synthase level and mitochondrial protein content in KO mstn muscle. Interestingly, mitochondrial enzyme activity and the cardiolipin fraction in the mitochondrial membrane are increased by training only in KO mstn mice. In conclusion, these results suggest that the combination of mstn inhibition and endurance training could increase the muscle mass while preserving the physical performance. In addition, cardiolipin and lipid-related pathways could represent new targets to improve mstn-deficient muscle metabolism and restore mitochondrial function.
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Submitted on : Wednesday, June 6, 2018 - 5:20:37 PM
Last modification on : Thursday, July 2, 2020 - 1:59:42 PM
Long-term archiving on: : Friday, September 7, 2018 - 3:06:14 PM


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  • HAL Id : tel-01809521, version 1



Narjes Baati. Le métabolisme lipidique dans les altérations mitochondriales induites par l’absence de myostatine : impact de l’entrainement en endurance. Education. Université Montpellier, 2018. Français. ⟨NNT : 2018MONT4002⟩. ⟨tel-01809521⟩



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