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Fatty Acid Changes in Liver Produced by Protein Deficiency and by Methionine or Cystine Fed to Rats in a Protein-free Ration

Laboratory of Nutrition and Endocrinology, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland

Liver fatty acid changes were studied during the development of an uncomplicated protein deficiency and in protein deficiency complicated by the addition of 0.30% methionine to the protein-free diet. (Only slightly fatty livers are produced in uncomplicated protein deficiency, whereas very fatty livers are produced by including methionine or cystine in a protein-free diet.) In general the fatty acid changes in adult male rats fed either diet followed similar patterns, although the extent of the changes was different. The increase in liver fatty acids could be accounted for almost entirely by elevations in palmitate, oleate, and linoleate. When dietary fat (corn oil) was omitted, however, the contribution by linoleate was depressed almost completely, being substituted for by palmitoleate and oleate. Significant loss of all fatty acids from the phospholipid fraction occurred. The presence of methionine in the protein-free diet in general protected against the loss of fatty acids from this fraction. Palmitoleate and oleate substituted for linoleate in the phospholipid fraction when dietary corn oil was omitted. The fat in the fatty livers produced by methionine or cystine was accounted for almost entirely by marked increases in neutral lipid palmitate, oleate, and linoleate. Cystine, methionine, and valine fed in the protein-free diet increased arachidonate concentration in the neutral lipid fraction, whereas leucine depressed it almost completely. When protein repletion was begun, all fatty acids except linoleate and arachidonate returned to extremely high values in the livers of the protein-free rats and to a much less extent in livers of the rats previously fed methionine in the protein-free diet. These studies suggest the following general conclusions: An as yet unknown mechanism allows the production of fatty livers when methionine is present in a protein-free ration. If linoleate is present in the diet, it accounts for a large part of the fat; but palmitoleate and oleate can substitute for linoleate. An imbalance between fat-synthesizing systems and fat-secreting systems in the liver probably accounts for a very large, transient increase in fatty acid concentrations when protein is reintroduced into the diet of protein-deficient animals. The enzyme systems involved in producing arachidonate from linoleate appear to be sharply impaired by protein deficiency. Methionine fed in a protein-deficient diet, however, almost completely prevents this effect.