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Mitochondrial fatty acid biosynthesis and muscle fiber plasticity in very long‐chain acyl‐CoA dehydrogenase‐deficient mice
Author(s) -
Tucci Sara,
Mingirulli Nadja,
Wehbe Zeinab,
Dumit Verónica I.,
Kirschner Janbernd,
Spiekerkoetter Ute
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12940
Subject(s) - beta oxidation , biochemistry , glycolysis , dehydrogenase , downregulation and upregulation , acyl coa dehydrogenase , lipoic acid , biosynthesis , skeletal muscle , fatty acid , long chain fatty acid , biology , mitochondrion , chemistry , metabolism , endocrinology , medicine , enzyme , gene , antioxidant
The white skeletal muscle of very long‐chain acyl‐CoA‐dehydrogenase‐deficient ( VLCAD −/− ) mice undergoes metabolic modification to compensate for defective β‐oxidation in a progressive and time‐dependent manner by upregulating glucose oxidation. This metabolic regulation seems to be accompanied by morphologic adaptation of muscle fibers toward the glycolytic fiber type II with the concomitant upregulation of mitochondrial fatty acid biosynthesis ( mFASII ) and lipoic acid biosynthesis. Dietary supplementation of VLCAD −/− mice with different medium‐chain triglycerides over 1 year revealed that odd‐chain species has no effect on muscle fiber switch, whereas even‐chain species inhibit progressive metabolic adaptation. Our study shows that muscle may undergo adaptive mechanisms that are modulated by dietary supplementation. We describe for the first time a concomitant change of mFASII in this muscular adaptation process.