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Nutritional encephalomalacia in the chick: an exposure of the vulnerable period for cerebellar development and the possible need for both ω6- and ω3-fatty acids

Published online by Cambridge University Press:  09 March 2007

P. Budowski
Affiliation:
Nuffield Laboratories of Comparative Medicine, Institute of Zoology, Regent's Park, London NWI 4RY
M. J. Leighfield
Affiliation:
Nuffield Laboratories of Comparative Medicine, Institute of Zoology, Regent's Park, London NWI 4RY
M. A. Crawford
Affiliation:
Nuffield Laboratories of Comparative Medicine, Institute of Zoology, Regent's Park, London NWI 4RY
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Abstract

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1. Cockerels (1-d-old) received over a period of 4 weeks, a balanced diet containing either safflower oil (diet S) or linseed oil (diet L) as a source of polyunsaturated fatty acids (PUFA). Body-weight, and weights of cerebrum and cerebellum increased at similar rates in the two dietary groups. The total fatty acids (FA) of the cerebellum differed from the cerebral FA by their higher PUFA and oleic acid contents and their lower stearic acid level. During the 3rd week of life there was a spurt in accretion of PUFA in the cerebellum, but not in the cerebrum. At the end of the experimental period phosphatidylethanolamine was present at twice the concentration in the cerebellum, compared with the cerebrum.

2. Diets S and L resulted in extensive mutual replacement of ω6- and ω3-FA in brain, without any significant change in the total PUFA. Brain oleic acid concentration was higher in the diet-L group than in the diet-S group, but saturated FA were not affected by the dietary treatments.

3. These results may be relevant to basic brain biology and to chick nutritional encephalomalacia (NE). This disease, which specifically affects the cerebellum and is readily induced by diets supplying linoleic acid but deficient in vitamin E, usually reaches its highest incidence during the 3rd week of life and may thus be related to the cerebellar PUFA spurt that occurs at that time. The fact that NE was induced by linoleic acid, while α-linolenic acid exerted a protective action, points to an overproduction of arachidonic-derived eicosanoids as a factor in the etiology of the cerebellar lesion and possibly a structural change due to a loss of docosahexaenoic acid and gain of arachidonic acid in the chicks given diet S.

Type
General Nutrition papers
Copyright
Copyright © The Nutrition Society 1987

References

REFERENCES

Budowski, P., Bartov, I., Drosr, Y. & Frankel, E. N. (1979). Lipids 14, 768780.CrossRefGoogle Scholar
Budowski, P., Hawkey, C. M. & Crawford, M. A. (1980). Annales de la Nutrition et de I'Alimentation 34, 389400.Google Scholar
Century, B. & Horwitt, M. K. (1959). Proceedings of the Society for Experimental Biology and Medicine 102, 375377.CrossRefGoogle Scholar
Century, B., Horwitt, M. K. & Bailey, P. (1959). American Medical Association's Archives of General Psychiatry 1, 420424.Google Scholar
Century, B., Witting, L. A., Harvey, C. C. & Horwitt, M. K. (1963). American Journal of Clinical Nutrition 13, 362368.CrossRefGoogle Scholar
Claeys, M., Wechsung, E., Herman, A. G. & Nugteren, D. H. (1981). Prostaglandins 21, 739749.CrossRefGoogle Scholar
Crawford, M. A., Casperd, N. M. & Sinclair, A. J. (1976). Comparative Biochemistry and Physiology 54b, 395401.Google Scholar
Dam, H., Nielsen, G. K., Prange, I. & Sondergaard, E. (1958). Nature 182, 802803.CrossRefGoogle Scholar
Dam, H. & Sondergaard, E. (1962). Zeitschrift für Ernaehrungswissenschaft 2, 217222.Google Scholar
Dobbing, J. (1972). In Lipids, Malnutrition and the Developing Brain, Ciba Foundation Symposium, pp. 920 [Elliott, K. and Knight, J., editors]. Amsterdam: Elsevier.Google Scholar
Dror, Y., Budowski, P., Bubis, J. J., Sandbank, U. & Wolman, M. (1976). In Progress in Neuropathology, vol. 3, pp. 343357 [Zimmerman, H. M., editor]. New York: Grune & Stratton.Google Scholar
Horwitt, M. K., Harvey, C. C. & Century, B. (1959). Science 130, 917918.Google Scholar
Machlin, L. J. & Gordon, R. S. (1960). Proceedings of the Society for Experimental Biology and Medicine 103, 659663.CrossRefGoogle Scholar
Marco, G. J., Machlin, L. J., Emery, E. & Gordon, R. S. (1961). Archives of Biochemistry and Biophysics 94, 115120.CrossRefGoogle Scholar
Mohrhauer, H. & Holman, R. T. (1963). Journal of Lipid Research 4, 151159.CrossRefGoogle Scholar
Neuringer, M., Connor, W. E., Lin, D. E., Barstad, L. & Luck, S. (1986). Proceedings of the National Academy of Science, USA 83, 40214025.CrossRefGoogle Scholar
Nouvelot, A., Bourre, J. M., Sezille, G., Dewailly, P. & Jaillard, J. (1983 a). Annals of Nutrition and Metabolism 27, 173181.CrossRefGoogle Scholar
Nouvelot, A., Dedonder-Decoopman, E., Sezille, G., Paturneau-Jouas, M., Dumont, O., Masson, M. & Bourre, J. M. (1983 b). Annals of Nutrition and Metabolism 27, 233240.Google Scholar
Pappenheimer, A. M. & Goettsch, M. (1931). Journal of Experimental Medicine 53, 1126.Google Scholar
Sinclair, A. J. & Crawford, M. A. (1973). British Journal of Nutrition 29, 127137.CrossRefGoogle Scholar
Sinnhuber, R. O., Castell, J. D. & Lee, D. J. (1972). Federation Proceedings 31, 14361441.Google Scholar
Subbiah, M. T. R., Deitemeyer, D. & Yunker, R. (1980). Thrombosis and Haemostasis (Stuttgart) 43, 189191.Google Scholar
Tinoco, J., Babcock, R., Hincenbergs, I., Medwadowski, B. & Miljanich, P. (1978). Lipids 13, 617.CrossRefGoogle Scholar
Vitiello, F. & Zanetta, J.-P. (1978). Journal of Chromatography 166, 637640.Google Scholar
Warso, M. A. & Lands, W. E. M. (1983). British Medical Bulletin 39, 277280.CrossRefGoogle Scholar