Plasma lipid changes in PRCD-affected and normal miniature poodles given oral supplements of linseed oil. Indications for the involvement of n-3 fatty acids in inherited retinal degenerations.

Abstract It has previously been shown that miniature poodles with progressive rod-cone degeneration (PRCD) have lower plasma levels of docosahexaenoic acid (22:6n-3) than normal poodles and it has been suggested that affected animals have a defect in the metabolism of 22:6n-3. To test this hypothesis in vivo, PRCD-affected and normal miniature poodles were given daily oral supplements of linseed oil (enriched in 18:3n-3). Blood was drawn from food-deprived animals at predetermined times before, during and after supplementation, and plasma lipid fatty acids were analysed. There were no differences in the levels of 18:3n-3, 20:5n-3, and 22:5n-3 between affected and normal dogs. Therefore, there appears to be no abnormality in the elongation and desaturation system that takes 18:3n-3 to 22:5n-3. Surprisingly, the plasma level of 22:6n-3 was reduced in both groups following supplementation, but to a significantly greater extent in affected dogs. This resulted in a significantly higher 22:5n-3/22:6n-3 ratio in affected animals. These results support the earlier suggestion of an abnormality in 22:6n-3 metabolism in PRCD-affected miniature poodles. To determine the effect of n-3 supplementation on polyunsaturated fatty acid metabolism in dogs (not as a function of disease), results from both groups of dogs were pooled and compared at times before and near the end of supplementation. Dietary 18:3n-3 led to predictable increases in 18:3n-3, 20:5n-3, and 22:5n-3, but to a decrease in 22:6n-3. There was no effect of supplementation on 18:2n-6 and 22:5n-6 levels, although the levels of 20:4n-6 and 22:4n-6 were lowered. These results show that short-term supplementation of n-3 fatty acids affects both n-3 and n-6 fatty acid metabolism in dogs, as reflected in changes in plasma fatty acids.