EFFECT OF VITAMIN-E TREATMENT ON TISSUE FATTY-ACIDS AND CHOLESTEROL CONTENT IN EXPERIMENTAL DIABETES

The effects of 8 months of a pharmacological dose of vitamin E were studied on cholesterol content and fatty acid distribution in streptozotocin-diabetic rats under a controlled diet. Diabetes induced a decrease of monounsaturated fatty acids and particularly palmitoleic acid in all studied tissues: liver, aorta, plasma (P < 0.01, P < 0.05, P < 0.05, respectively). Vitamin E corrected partially Delta 9 desaturase activity and consequently enhanced monounsaturated acids in all tissues. Concerning fatty acids of the n-6 series, diabetes induced an increase of C18:3 n-6 and C20:4 n-6 in liver associated with an overcorrection of Delta 6 and Delta 5 desaturase activities. Vitamin E normalized Delta 6 activity in liver, and in aorta increased significantly C20:3 n-6 and C20:4 n-6 (P < 0.005, P < 0.005), which are fatty acid precursors of PGE1 and PG12, prostaglandins protective for vessels. Fatty acids of the n-3 series decreased in the liver except C22:6 n-3; vitamin E again prevented these changes and increased in the aorta C22:5 n-3 and C22:6 n-3, which are involved in the generation of PG13 whose activity is additive to PG12. In plasma, polyunsaturated fatty acid pattern modifications were very similar to those of liver. Vitamin E was also able to prevent the decrease of free and esterified cholesterol observed in diabetic liver. Moreover, an increase of cholesterol in diabetic aorta was also modulated by vitamin E. Vitamin E could protect the long chain of polyunsaturated fatty acids, thereby preserving the physical properties of membranes and the environment necessary for enzymatic activities involved in fatty acid and cholesterol metabolism. Further, vitamin E in the aorta, by maintaining a high percentage of fatty acid precursors of protective prostaglandins, could represent an interesting therapy in diabetes to prevent atheroma.