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A STUDY OF THE EFFECT OF CREATINE ON GROWTH AND ITS DISTRIBUTION IN THE TISSUES OF NORMAL RATS

A. Chanutin

Published 1927 in Journal of Biological Chemistry

ABSTRACT

The idea that creatine might serve as a food was first advanced by Folin (1). The evidence for this suggestion was based on the failure to recover or account for small amounts of ingested creatine. Benedict and Osterberg (2), in a series of experiments with dogs, demonstrated conclusively that ingested creatine is partially retained, and apparently utilized by the organism, and that dogs fed creatine showed an increase in weight and a positive nitrogen balance. It was shown by Chanutin(3) that a positive nitrogen balance follows creatine feeding in man. It has been suggested (2,3) that creatine may be responsible for the gains in weight noted in the experimental subjects. Since creatine occurs in practically all the tissues of the body, it may be assumed that it plays a Ale in normal metabolism. Despite the general distribution of this substance, there is evidence that the muscles and liver are chiefly concerned in its metabolism. These tissues have been investigated principally in relation to the storage of creatine. In many of the experiments reported in the literature, data were obtained from subjects stiering with obscure pathological conditions such as muscular dystrophy or hepatic diseases. In some cases these abnormal conditions have rendered interpretation diflicult or impossible. Mellanby (4) has presented evidence which indicates that the liver is intimately associated with creatine metabolism. This investigator found that the muscle creatine of the chick embryo appears and increases synchronously with the development and growth of the liver. Furthermore, he states that although the cross-striated muscles of the invertebrates are histologically identical with those of the vertebrates, creatine is absent from the tissues of the lower forms because there is no organ present which corresponds to the liver of the vertebrates. Mellanby has added more data to support his contention by studying the creatine and creatinine output in people suffering from liver affections. He found that creatinine excretion is diminished in certain types of hepatic disease, and has suggested that the liver is responsible for the formation of creatinine. Chisholm (5), after

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