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2018-02-18 - Colloque/Présentation - poster - Anglais - 1 page(s)

Dudome Virginie , Coppée Frédérique , Declèves Anne-Emilie, "Lipotoxicity and oxidative stress induced by palmitate in human muscle cells" in Scientific Meeting FNRS Contact Group "Oxidative Processes and Antioxidants" , Namur, Belgique, 2018

  • Codes CREF : Biologie cellulaire (DI311D)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
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Abstract(s) :

(Anglais) Lipotoxicity and oxidative stress induced by palmitate in human muscle cells V. DUDOME, S.GENVA, F.COPPEE and A-E DECLEVES Laboratoire de Biologie Moléculaire, Université de Mons, Mons,Belgium. Accumulation of saturated fatty acids contributes to lipotoxicity-related skeletal muscle dysfunction. Particularly, oxidative stress has been considered as a trigger of muscle insulin resistance and atrophy. Even though it is well established that reactive oxygen species (ROS) are mainly produced by mitochondria, less is known regarding which are the main source of mitochondrial ROS. Therefore, our study investigated the effects of high level of saturated fatty acid on mitochondrial ROS production and NADPH oxidase expression using human skeletal muscle cells. To do so, myoblast and differentiated human skeletal cells were used at different stages of differentiation. The effect of palmitate (PA-300µM) on cell viability, intracellular lipid accumulation, expression of NADPH oxidase subunits and balance between oxidative stress and antioxidants were determined. PA caused a significant increase in intracellular lipid droplets along with the significant rise in mitochondrial superoxide in myoblast and differentiated myotubes. However, there were no change in NOX2, NOX4, p22Phox and p47phox expression at the mRNA level. Moreover, our observations were concomitant to increased catalase and NRF2 protein expression. In summary, these results provide new information regarding PA-induced lipotoxicity in human skeletal muscle cells. Particularly, the PA induced increased superoxide level from mitochondria. Interestingly, antioxidant defenses were also increased. This highlights a protective response from human muscle cells against oxidative insult.