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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

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