Long chain fatty acid deficits in brain myelin sphingolipids of undernourished rat pups.

A restricted maternal dietary intake (40% of ad libitum intake) is known to cause myelin deficit that is accompanied by decreased amounts of individual phospholipids and sphingolipids in brain myelin of suckling rats. This communication reports the effects of the same nutritional stress on the fatty acid composition of brain myelin lipids. In myelin of 19-day-old normally fed rats, palmitate (16:0), stearate (18:0) and oleate (18:1) accounted for 80-90% of all fatty acids in phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine. Maternal dietary restriction resulted in deficits of total fatty acid content, but did not affect the proportional distribution of individual fatty acids among phospholipids. By contrast, longer chain (22- and 24-carbon) fatty acids accounted for more than half the fatty acid content of myelin cerebroside and sulfatide from the 19-day-old control rat pups. In undernourished rats of that age, proportions of lignocerate (24:0) and nervonate (24:1) in cerebroside and sulfatide were 40-50% lower than those in control rats. This, together with higher proportions of 16:0, 18:0 and 18:1 and a higher ratio of C16-C20 to C22-C24 in undernourished than in control rats, suggests an impairment in fatty acid chain elongation. Ten days of nutritional rehabilitation failed to restore the fatty acid imbalances; however, after an additional 5 days of ad libitum feeding, the experimental and control values were similar. The undernutrition results in hypomyelination, which is characterized by a proportional decrease in lignoceric and nervonic acids of sphingolipids.