Hostname: page-component-78c5997874-mlc7c Total loading time: 0 Render date: 2024-11-19T06:47:00.608Z Has data issue: false hasContentIssue false

Biochemical observations on rat aorta: interaction of dietary protein and cholesterol

Published online by Cambridge University Press:  09 March 2007

S. P. Bydlowski
Affiliation:
Lipid Research Center, University Hospital, K-Pavilion, 4th Floor, Mail Location 540, 234 Goodman Street, Cincinnati, Ohio 45267, USA
V. L. G. Stivaletti
Affiliation:
Laboratorio de Medicina Experimental, Department of Physiological Sciences, Faculdade de Ciencias Medicus da Sunta casa de Sao Paulo, Suo Paulo, SP, Brazil
C. R. Douglas
Affiliation:
Laboratorio de Medicina Experimental, Department of Physiological Sciences, Faculdade de Ciencias Medicus da Sunta casa de Sao Paulo, Suo Paulo, SP, Brazil
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. The effect of cholesterol feeding during and after a period of protein malnutrition lasting 4 weeks was examined in the rat. Indices measured were plasma total cholesterol, triglycerides and protein levels, and aorta total cholesterol, triglycerides, hexosamine and hydroxyproline concentrations.

2. In both plasma and aorta, total cholesterol and triglycerides levels were higher in the low-protein diet group than in the standard-protein diet group, when cholesterol was supplied in both diets.

3. During the malnutrition period, cholesterol feeding led to a greater decrease in plasma protein than that promoted by the low-protein diet without cholesterol, while aorta hexosamine levels decreased to a lesser extent.

4. Cholesterol feeding with a standard-protein diet promoted a slight and temporary increase in aorta hydroxyproline levels, while a decrease in aorta hexosamine concentration was observed. Cholesterol feeding with the low-protein diet, on the other hand, also promoted a decrease in aorta hexosamine levels but to a lesser extent.

5. During the recovery period, cholesterol feeding impaired the return of plasma protein, aorta hexosamine and lipid levels to that of the control values.

6. These findings demonstrate that cholesterol feeding promotes different changes in aorta and plasma, depending on whether or not protein is supplied by the diet in adequate amounts. This point could be important in relation to the development of atherosclerosis during recovery from a period of malnutrition.

Type
Papers of direct relevance to Clinical and Human Nutrition
Copyright
Copyright © The Nutrition Society 1986

References

REFERENCES

Bydlowski, S. P., Stivaletti, V. L. G. & Douglas, C. R. (1981 a). IRCS Medical Sciences 9, 743744.Google Scholar
Bydlowski, S. P., Stivaletti, V. L. G. & Douglas, C. R. (1981 b). IRCS Medical Sciences 9, 834.Google Scholar
Bydlowski, S. P., Stivaletti, V. L. G. & Douglas, C. R. (1981 c). IRCS Medical Sciences 9, 895.Google Scholar
Bydlowski, S. P., Stivaletti, V. L. G. & Douglas, C. R. (1981 d). In Advances of Physiological Sciences, vol. 5, pp. 185192 [Palkovic, M., editor]. New York: Pergamon Press.Google Scholar
Bydlowski, S. P., Stivaletti, V.L. G. & Douglas, C. R. (1983). IRCS Medical Sciences 11, 298299.Google Scholar
Bydlowski, S. P., Stivaletti, V. L. G. & Douglas, C. R (1984). Annals of Nutrition and Metabolism 28, 8591.CrossRefGoogle Scholar
Carlson, L. A. (1963). Journal of Atherosclerosis Research 3, 334336.CrossRefGoogle Scholar
Corraze, G., Lacombe, C. & Nibbelink, M. (1984). Lipids 19, 812814.Google Scholar
Deykin, D. & Goodman, D. S. (1962). Journal of Biological Chemistry 237, 36493651.CrossRefGoogle Scholar
Elson, L. A. & Morgan, W. T. J. (1933). Biochemistry 27, 18241828.Google Scholar
Fisher, H., Feigenbaum, A., Leveille, G. A., Weiss, H. S. & Griminger, P. (1959). Journal of Nutrition 69, 163171.CrossRefGoogle Scholar
Fitch, S. M., Harkness, M. L. R. & Harkness, R. D. (1955). Nature 176, 163.CrossRefGoogle Scholar
Folch, J., Lees, M. & Stanley, G. H. S. (1957). Journal of Biological Chemistry 226, 497509.CrossRefGoogle Scholar
Levy, R., Rifkind, B., Dennis, B. & Emst, N. (1979). Nutrition, Lipids and Coronary Heart Disease. New York: Raven Press.Google Scholar
Little, J. M. & Angell, E. A. (1977). Atherosclerosis 26, 173179.CrossRefGoogle ScholarPubMed
Lowry, O.H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). Journal of Biological Chemistry 193, 265275.CrossRefGoogle Scholar
Newman, R. E. & Logan, M. A. (1950). Journal of Biological Chemistry 184, 299306.CrossRefGoogle Scholar
Nikkila, E. A. & Ollila, O. (1957). Acta Pathologica Microbiologica Scandinavica 40, 177180.Google Scholar
Richard, M. J., Serbus, D. C., Beitz, D. C. & Jacobson, N. L. (1982). Nutrition Research 2, 175183.Google Scholar
Rimington, C. (1940). Biochemical Journal 34, 931940.CrossRefGoogle Scholar
Rosenthal, H. L., Pfluke, B. S. M. L. & Buscaglia, S. (1957). Journal of Laboratory and Clinical Medicine 50, 318322.Google Scholar
Saito, S. & Fillios, L. C. (1965). American Journal of PhysioIogy 208, 882886.CrossRefGoogle Scholar
Subbiah, M. T. R. (1977). Nutrition Reports International 15, 223229.Google Scholar
Subbiah, M. T. R. & Siekert, R. G. Jr (1979). British Journal of Nutrition 41, 16.Google Scholar
Wiggers, K. D., Richard, M. J., Stewart, J. W., Jacobson, N. L. & Berger, P. J. (1977). Atherosclerosis 27, 2734.CrossRefGoogle Scholar