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Journal of Nutrition Vol. 104 No. 6 June 1974, pp. 761-771
Copyright © 1974 by American Society for Nutrition
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Effect of Dietary Methionine Level on Its Metabolism in Rats1

T. S. Aguilar2, N. J. Benevenga and A. E. Harper

Departments of Meat and Animal Science and Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706

The metabolism of methyl- or carboxyl-labeled methionine was studied in young rats receiving diets that were deficient or adequate in methionine. The diets were unsupplemented or supplemented with cysteine so that the cysteine/methionine ratio was constant at 0.52 (mole/mole). As the methionine level increased from 0.2 to 0.8% of the diet, the calculated oxidation of methionine increased 10-fold whether the diet was unsupplemented or supplemented with cysteine. Approximately three times as much of the methyl carbon as the carboxyl carbon was recovered as CO2. Incorporation of the methyl group into liver and muscle protein and phospholipids increased two- to threefold whereas the incorporation of the carboxyl carbon into the protein of the liver and muscle was unchanged as methionine level increased from 0.2 to 0.8% of the diet. Cysteine supplementation appeared to have little effect on the incorporation. The ratio of incorporation of the methyl to carboxyl carbon of methionine into liver and plasma proteins indicated that the methionine methyl carbon is extensively turned over at low dietary levels of methionine. The metabolism of the methionine methyl group generates intermediates which are involved in the synthesis of serine since the radioactivity from the methionine methyl group recovered in serine and cysteine in plasma and liver proteins accounts for approximately one-third of the total radioactivity when dietary levels of methionine were 0.8% of the diet.


KEY WORDS: • methionine • cysteine • methyl metabolism

1 Supported by funds from the College of Agricultural and Life Sciences, University of Wisconsin, by a grant from the National Live Stock and Meat Board, Chicago, Illinois, and by Public Health Service Research Grant no. AM 15227.

2 Ford Foundation Fellow.

Manuscript received 13 December 1973.


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