This study was performed to determine whether
vitamin E supplementation in
streptozotocin-induced diabetic rats treated by
insulin could reduce serum oxidation markers (
malondialdehyde: MDA,
Schiff bases, anti-
protein-MDA adduct
antibodies) and modulate
lipid changes. After 10 weeks, diabetes induced in rats a significant increase in
Schiff bases (P < 0.006) and anti-
protein-MDA adduct
antibodies (P < 0.01). These alterations were accompanied by a significant rise in serum
free fatty acids (225%),
triglycerides (35%), and
phospholipids (30%) and changes in
fatty acid distribution in these fractions and in
cholesterol esters.
Vitamin E supplementation in diabetic rats reduced
Schiff bases and anti-
protein-MDA adduct
antibodies and tended to restore the
fatty acid profile close to control rats without decreasing quantitatively serum
lipids enhanced by diabetes. Concerning
fatty acids,
vitamin E chiefly reduced
stearic acid (C18:0) in
free fatty acids,
cholesterol esters, and
phospholipids and cancelled the decrease in low molecular
triglycerides observed in diabetic rats. Furthermore,
vitamin E maintained the ratio of monounsaturated and
polyunsaturated fatty acids, particularly with respect to
oleic acid (C18:1),
dihomo-gamma-linolenic acid (C20:3 n-6), eicosapentaenoic (C20:5 n-3), and
docosapentaenoic acid (C22:5 n-3), in serum
phospholipids. These changes observed in
vitamin E supplemented rats, compared to
vitamin E-untreated diabetic rats, could favor prevention of accelerated
atherogenesis. Particularly, the decrease of serum
peroxides and enhancement in
phospholipid fatty acids (C20:3 n-6, C20:5 n-3, and C22:5 n-3) could induce the preferential formation of
prostaglandins (
PGE1, PGI2,
PGI3) which are protective in
cardiovascular diseases.