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• W2939403926 abstract "Loss of long-chain acyl-CoA synthetase isoform-1 (ACSL1) in mouse skeletal muscle (Acsl1M−/−) severely reduces acyl-CoA synthetase activity and fatty acid oxidation. However, the effects of decreased fatty acid oxidation on skeletal muscle function, histology, use of alternative fuels, and mitochondrial function and morphology are unclear. We observed that Acsl1M−/− mice have impaired voluntary running capacity and muscle grip strength and that their gastrocnemius muscle contains myocytes with central nuclei, indicating muscle regeneration. We also found that plasma creatine kinase and aspartate aminotransferase levels in Acsl1M−/− mice are 3.4- and 1.5-fold greater, respectively, than in control mice (Acsl1flox/flox), indicating muscle damage, even without exercise, in the Acsl1M−/− mice. Moreover, caspase-3 protein expression exclusively in Acsl1M−/− skeletal muscle and the presence of cleaved caspase-3 suggested myocyte apoptosis. Mitochondria in Acsl1M−/− skeletal muscle were swollen with abnormal cristae, and mitochondrial biogenesis was increased. Glucose uptake did not increase in Acsl1M−/− skeletal muscle, and pyruvate oxidation was similar in gastrocnemius homogenates from Acsl1M−/− and control mice. The rate of protein synthesis in Acsl1M−/− glycolytic muscle was 2.1-fold greater 30 min after exercise than in the controls, suggesting resynthesis of proteins catabolized for fuel during the exercise. At this time, mTOR complex 1 was activated, and autophagy was blocked. These results suggest that fatty acid oxidation is critical for normal skeletal muscle homeostasis during both rest and exercise. We conclude that ACSL1 deficiency produces an overall defect in muscle fuel metabolism that increases protein catabolism, resulting in exercise intolerance, muscle weakness, and myocyte apoptosis. Loss of long-chain acyl-CoA synthetase isoform-1 (ACSL1) in mouse skeletal muscle (Acsl1M−/−) severely reduces acyl-CoA synthetase activity and fatty acid oxidation. However, the effects of decreased fatty acid oxidation on skeletal muscle function, histology, use of alternative fuels, and mitochondrial function and morphology are unclear. We observed that Acsl1M−/− mice have impaired voluntary running capacity and muscle grip strength and that their gastrocnemius muscle contains myocytes with central nuclei, indicating muscle regeneration. We also found that plasma creatine kinase and aspartate aminotransferase levels in Acsl1M−/− mice are 3.4- and 1.5-fold greater, respectively, than in control mice (Acsl1flox/flox), indicating muscle damage, even without exercise, in the Acsl1M−/− mice. Moreover, caspase-3 protein expression exclusively in Acsl1M−/− skeletal muscle and the presence of cleaved caspase-3 suggested myocyte apoptosis. Mitochondria in Acsl1M−/− skeletal muscle were swollen with abnormal cristae, and mitochondrial biogenesis was increased. Glucose uptake did not increase in Acsl1M−/− skeletal muscle, and pyruvate oxidation was similar in gastrocnemius homogenates from Acsl1M−/− and control mice. The rate of protein synthesis in Acsl1M−/− glycolytic muscle was 2.1-fold greater 30 min after exercise than in the controls, suggesting resynthesis of proteins catabolized for fuel during the exercise. At this time, mTOR complex 1 was activated, and autophagy was blocked. These results suggest that fatty acid oxidation is critical for normal skeletal muscle homeostasis during both rest and exercise. We conclude that ACSL1 deficiency produces an overall defect in muscle fuel metabolism that increases protein catabolism, resulting in exercise intolerance, muscle weakness, and myocyte apoptosis." @default.
• W2939403926 created "2019-04-25" @default.
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• W2939403926 date "2019-05-01" @default.
• W2939403926 modified "2023-10-15" @default.
• W2939403926 title "Defective fatty acid oxidation in mice with muscle-specific acyl-CoA synthetase 1 deficiency increases amino acid use and impairs muscle function" @default.
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• W2939403926 cites W1601325022 @default.
• W2939403926 cites W1799278215 @default.
• W2939403926 cites W1920067934 @default.
• W2939403926 cites W1921425544 @default.
• W2939403926 cites W1934325817 @default.
• W2939403926 cites W1935072652 @default.
• W2939403926 cites W1963910480 @default.
• W2939403926 cites W1966170191 @default.
• W2939403926 cites W1986813347 @default.
• W2939403926 cites W1989689747 @default.
• W2939403926 cites W1998118119 @default.
• W2939403926 cites W2001548627 @default.
• W2939403926 cites W2004655740 @default.
• W2939403926 cites W2013072437 @default.
• W2939403926 cites W2017429680 @default.
• W2939403926 cites W2019863019 @default.
• W2939403926 cites W2020444654 @default.
• W2939403926 cites W2030802624 @default.
• W2939403926 cites W2030901818 @default.
• W2939403926 cites W2033804400 @default.
• W2939403926 cites W2035527647 @default.
• W2939403926 cites W2054248098 @default.
• W2939403926 cites W2063121632 @default.
• W2939403926 cites W2068411103 @default.
• W2939403926 cites W2072152524 @default.
• W2939403926 cites W2079386976 @default.
• W2939403926 cites W2089019519 @default.
• W2939403926 cites W2090030503 @default.
• W2939403926 cites W2106592023 @default.
• W2939403926 cites W2110542127 @default.
• W2939403926 cites W2115432680 @default.
• W2939403926 cites W2117940735 @default.
• W2939403926 cites W2119901011 @default.
• W2939403926 cites W2125392951 @default.
• W2939403926 cites W2125404675 @default.
• W2939403926 cites W2127247844 @default.
• W2939403926 cites W2127498339 @default.
• W2939403926 cites W2129377253 @default.
• W2939403926 cites W2132489811 @default.
• W2939403926 cites W2133793013 @default.
• W2939403926 cites W2134373383 @default.
• W2939403926 cites W2138521217 @default.
• W2939403926 cites W2139098448 @default.
• W2939403926 cites W2141879632 @default.
• W2939403926 cites W2144959011 @default.
• W2939403926 cites W2151698573 @default.
• W2939403926 cites W2159545287 @default.
• W2939403926 cites W2160524748 @default.
• W2939403926 cites W2168526937 @default.
• W2939403926 cites W2292988270 @default.
• W2939403926 cites W2300552860 @default.
• W2939403926 cites W2301336672 @default.
• W2939403926 cites W2325707043 @default.
• W2939403926 cites W2337937249 @default.
• W2939403926 cites W2405756572 @default.
• W2939403926 cites W2431575019 @default.
• W2939403926 cites W2464639360 @default.
• W2939403926 cites W2480163530 @default.
• W2939403926 cites W2521855531 @default.
• W2939403926 cites W2590600658 @default.
• W2939403926 cites W2592680415 @default.
• W2939403926 cites W2773666593 @default.
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• W2939403926 doi "https://doi.org/10.1074/jbc.ra118.006790" @default.
• W2939403926 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6552438" @default.
• W2939403926 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30975900" @default.
• W2939403926 hasPublicationYear "2019" @default.
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