Vitamin E deficiency and metabolism of amino acids in skeletal muscle

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Abstract
Hemidiaphragms or slices of skeletal muscle from vitamin E-deficient and control rabbits were incubated with glycine-C14, leucine-Cl4, or lysine-Cl4. Vitamin E deficiency increased the labeling of protein not just by glycine, as in vivo, but by each of the 3 amino acids[long dash]at least eightfold in slices and twofold in hemidiaphragms. Thus, the abnormal metabolism of amino acids in muscle is not limited to glycine. Experiments with skeletal muscle slices from rabbits developing vitamin E deficiency showed that histologic changes precede the increase in the labeling of protein. Vitamin E treatment of vitamin E-deficient rabbits did not immediately correct the increased labeling of protein of hemidiaphragms by glycine-C14; at least 9-12 days of treatment were required. The abnormality is a secondary response to vitamin E deficiency.