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Effects on liver and serum lipids of dietary supplements of methionine and excess lysine given to previously-starved rats

Published online by Cambridge University Press:  24 July 2007

Yoritaka Aoyama ,
Kazuhiro Sakaida ,
Akira Yoshida  and
Kiyoshi Ashida
Yoritaka Aoyama
Affiliation:
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Furo-cho, Chikusa, Nagoya, Japan
Kazuhiro Sakaida
Affiliation:
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Furo-cho, Chikusa, Nagoya, Japan
Akira Yoshida
Affiliation:
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Furo-cho, Chikusa, Nagoya, Japan
Kiyoshi Ashida
Affiliation:
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Furo-cho, Chikusa, Nagoya, Japan
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Abstract

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1. The addition of lysine hydrochloride (50 g/kg) to a diet supplemented with methionine (3 g/kg) had no effect on liver lipids when rats (Wistar and Sprague-Dawley) were fed ad lib. for 14 d. However, refeeding a diet supplemented with methionine and excess lysine hydrochloride to previously-starved rats (Wistar) for 6, 7 or 9 d, but not 3 or 4 d, resulted in liver lipid accumulation, mainly triglycerides, which was prevented by the addition of arginine, citrulline, ornithine, adenine, allopurinol or maize oil, but not by guanine, cytosine, thymine or uracil.

2. The addition of lysine hydrochloride to a methionine-supplemented diet resulted in reduced serum triglyceride levels after refeeding for 3 or 4 d and reduced serum cholesterol levels after refeeding for 3, 4 or 6 d. Serum lipids were unaffected by refeeding the diets for 7 or 9 d.

3. Since hepatic lipid accumulation was preceded by the decline in the level of serum triglycerides, one of the factors responsible for lipid accumulation in the liver might be reduced transport of triglycerides from the liver into the blood.

4. When adenine and allopurinol were added to the diet supplemented with methionine and lysine hydrochloride refed for 4 d, there was an increase in serum triglycerides. However, when this diet was refed for 7 d, with the addition of arginine, citrulline, guanine, pyrimidine bases, allopurinol or maize oil, no effects on serum cholesterol and triglyceride levels were observed.

Type
Research Article
Information
British Journal of Nutrition , Volume 50 , Issue 3 , November 1983 , pp. 627 - 636
Copyright
Copyright © The Nutrition Society 1983

References

Aoyama, Y. & Ashida, K. (1979). Nutrition Reports International 20, 483–490.Google Scholar
Aoyama, Y., Izumichi, T., Sakakibara, H., Yoshida, A. & Ashida, K. (1975). Nutrition Reports International 12, 163–173.Google Scholar
Aoyama, Y., Yasui, H. & Ashida, K. (1971). Journal of Nutrition 101, 739–745.CrossRefGoogle Scholar
Aoyama, Y., Yoshida, A. & Ashida, K. (1981). Journal of Nutrition 111, 895–906.CrossRefGoogle Scholar
Barlet, G. R. (1959). Journal of Biological Chemistry 234, 466–468.CrossRefGoogle Scholar
Creasey, W. A., Hankin, L. & Handschumacher, R. E. (1961). Journal of Biological Chemistry 236, 2064–2070.CrossRefGoogle Scholar
Duncan, D. B. (1955). Biometrics 11, 1–42.CrossRefGoogle Scholar
Feigelson, P., Davidson, J. D. & Robins, R. K. (1957). Journal of Biological Chemistry 226, 993–1000.CrossRefGoogle Scholar
Folch, J., Lees, M. & Sloane Stanley, G. H. (1957). Journal of Biological Chemistry 226, 497–509.CrossRefGoogle Scholar
Fyfe, J. A., Nelson, D. J. & Hitching, G. H. (1974). Advances in Experimental Medicine and Biology 41B, 621–628.CrossRefGoogle Scholar
Handschumacher, R. E., Creasey, W. A., Jaffe, J. J., Pasternak, C. A. & Hankin, L. (1960). Proceedings of the National Academy of Sciences of the USA 36, 178–186.CrossRefGoogle Scholar
Hevia, P., Kari, F. W., Ulman, E. A. & Visek, W. J. (1980 a). Journal of Nutrition 110, 1224–1230.CrossRefGoogle Scholar
Hevia, P., Ulman, E. A., Kari, F. W. & Visek, W. J. (1980 b). Journal of Nutrition 110, 1231–1239.CrossRefGoogle Scholar
Hevia, P. & Visek, W. J. (1980). Lipids 15, 95–99.CrossRefGoogle ScholarPubMed
Lombardi, B., Ugazio, G. & Raick, A. (1966). American Journal of Physiology 210, 31–36.CrossRefGoogle Scholar
Milner, J. A. (1979). Journal of Nutrition 109, 663–670.CrossRefGoogle Scholar
Milner, J. A. & Perkin, E. G. (1978). Lipids 13, 563–565.CrossRefGoogle Scholar
Milner, J. A. & Visek, W. J. (1975). Metabolism 24, 643–651.CrossRefGoogle Scholar
Muto, Y. & Gibson, D. M. (1970). Biochemical and Biophysical Research Communications 38, 9–15.CrossRefGoogle Scholar
Pearson, S., Stern, S. & McGavack, T. H. (1953). Analytical Chemistry 25, 813–814.CrossRefGoogle Scholar
Sabine, J. R., McGrath, H. & Abraham, S. (1969). Journal of Nutrition 98, 312–318.CrossRefGoogle Scholar
Standerfer, S. B. & Handler, P. (1955). Proceedings of the Society for Experimental Biology and Medicine 90, 270–271.CrossRefGoogle Scholar
Ugazio, G. & Lombardi, B. (1965). Laboratory Investigation 14, 711–719.Google Scholar
Ulman, E. A., Kari, F. W., Hevia, P. & Visek, W. (1981). Journal of Nutrition 111, 1772–1779.CrossRefGoogle Scholar
Wahlefeld, A. W. (1974). Methods of Enzymatic Analysis 4, 1831–1835.CrossRefGoogle Scholar
Windmueller, H. G. & Spaeth, A. E. (1966). Journal of Biological Chemistry 241, 2891–2899.CrossRefGoogle Scholar
Windmueller, H. G. & von Euler, L. H. (1971). Proceedings of the Society for Experimental Biology and Medicine 136, 98–101.CrossRefGoogle Scholar