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Fat Deficiency in Rats during Development of the Central Nervous System and Susceptibility to Experimental Allergic Encephalomyelitis1

Daniel P. Selivonchick2, 3, and Patricia V. Johnston

Department of Food Science, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801

On day 14 of gestation, Sprague-Dawley rats were assigned to a diet adequate in fat (C), a fat-deficient diet (FD), or a fat-deficient diet supplemented with ethyl linoleate (FD-S). The same diets were continued during lactation. On weaning, the offspring were fed the same diets as their mothers. Rats were killed at 21 and 33 days, and the lipid compositions of brain, brain myelin, and spinal cord myelin were determined. Experimental allergic encephalomyelitis (EAE) was induced in animals from each group at 54 days of age. Acute EAE occurred after 13 days, and on day 14 (day 68 of age), the rats were killed. Body, brain, and brain myelin developments were slower in the FD and FD-S rats during early life. At 68 days, brain myelin from all groups reached mature composition, although body and brain weights of FD and FD-S rats remained lower than those of controls. With the exception of a slightly lower plasmalogen content at 33 and 68 days, the composition of spinal cord myelin from FD and FD-S rats was similar to that of C rats throughout the period of study. The greatest incidence and severity of EAE occurred in animals from the FD group. The incidence of the disease in FD-S rats was similar to that in the controls. A reduction in total brain protein occurred in FD-EAE rats and in C-EAE and FD-EAE cerebrosides. Myelin from brain and spinal cord of EAE rats did not differ appreciably in protein content or lipid composition from myelin of controls. It was concluded that fat deficiency during development leads to increased susceptibility to EAE, and that a supplement of a source of linoleic acid has a marked protective effect against EAE.


KEY WORDS: • essential fatty acids • experimental allergic encephalomyelitis • multiple sclerosis

1 Supported by Public Health Service Research Grant number HD 05204 from the National Institute of Child Health and Human Development.

2 Part of a dissertation submitted by Daniel P. Selivonchick to the University of Illinois in a partial fulfillment of the requirements for the Ph.D. degree.

3 Present address: Department of Zoology, Erindale College, University of Toronto, Clarkson, Ontario, Canada.

Manuscript received 10 January 1974.





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