The creatine content of the liver in the muscular dystrophy of vitamin E deficiency.

Creatinuria is one of the results of vitamin E deficiency. This was first demonstrated by Morgulis and Spencer (1) on rabbits. The effectiveness of a-tocopherol in reducing the excretion of creatine to normal levels was shown by Mackenzie and McCollum (2) and has been verified by many others. The creatine lost from muscle tissue during dystrophy (3) undoubtedly accounts for the creatinuria, and the administration of Qtocopherol prevents this loss (4). Biopsy experiments on dystrophic rabbits (5) indicated that the restoration of normal muscle creatine content, after the administration of tocopherol phosphate by vein, was delayed some hours as compared with relatively prompt reduction of the high oxygen consumption. This latter dropped in about 4 hours, whereas the already low creatine content was initially still further reduced. A suggested explanation for these changes was that the loss of creatine from muscle continued, while a previously accelerated process of synthesis had already been depressed. There is no proof that the synthesis of creatine is accelerated in dystrophic animals, but the high rate of excretion would quickly exhaust the existing stores unless these were being replenished at a greater than normal rate.’