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Fatty infiltration of the liver may be produced experimentally in animals by various means, including dietary restriction of proteins, of choline or choline precursors, or of vitamins, as well as the use of hepatotoxins (1). The lesions produced may progress to a pathologic picture resembling that of cirrhosis in human beings. Although it is not universally agreed that the pathogenesis of human cirrhosis is similar to that in animals, many investigators have felt that fatty infiltration represents an intermediate phase, which, while reversible, may also progress to cirrhosis. It has been noted in experimental animals that methionine and choline have a lipotropic action, preventing the deposition of fat in the liver as well as enhancing its removal (2). This effect is thought to result from an increase in the formation and the turnover of phospholipides (3). Indeed, in experimental animals with fatty infiltration of the liver induced by diet, it has been shown by the use of radiophosphorus that choline or methionine will cause an increase in the phospholipide turnover in the liver (4, 5). In human beings the therapeutic value of choline and methionine in the treatment of certain forms of chronic hepatitis, with or without the presence of fatty infiltration of the liver, is open to question (6). Numerous observers have noted a reduction in liver size and both clinical and laboratory evidence of improvement which they felt could be attributed directly to the use of choline or

the journal of clinical investigation/the journal of clinical investigation

THE EFFECTS OF LIPOTROPIC FACTORS ON PHOSPHOLIPIDE TURNOVER IN THE PLASMA OF PATIENTS WITH CIRRHOSIS OF THE LIVER, AS INDICATED BY RADIOACTIVE PHOSPHORUS 1