Muscle fiber-type switch in acyl-CoA synthetase-1 knockout mice

The product of the Acsl1 gene activates fatty acids for β-oxidation in aerobic respiration. Without ACSL1, type I fibers, which primarily depend on fatty acids, may not be able to produce energy. In this study, we have shown that muscle-specific ACSL1 is important in skeletal muscle fiber type and structure. Mice with muscle-specific Acsl1 deletions developed centronuclear myopathies, accompanied by an increase in creatine kinase activity and myofiber conversion from glycolytic to oxidative. To investigate this myofiber conversion, molecular activators of PGC1α, such as SIRT1 and AMPK, were measured but we found that their role is not significant. Our findings reveal an essential role of ACSL1 in myofiber identity, skeletal muscle structure, and development of centronuclear myopathies.Bachelor of Science in Public Healt