Prevention of nerve conduction deficit in diabetic rats by polyunsaturated fatty acids1,2,3
Prevention of nerve conduction deficit in diabetic rats by polyunsaturated fatty acids1,2,3
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Richard J Head, Peter L McLennan, Daniel Raederstorff, Reto Muggli, Sharon L Burnard and Edward J McMurchie
1 From the CSIRO, Human Nutrition, Adelaide, Australia, and F Hoffmann-La Roche AG, Vitamin Research and Technology Department, Basel, Switzerland.
The influence of diets containing -linolenic acid (GLA; 18:3n-6) on sciatic nerve conduction velocity (NCV) was determined in diabetic rats. NCV was lower in diabetic rats fed diets supplemented with olive oil or sunflower seed oil than in nondiabetic rats; rats supplemented with GLA during a 5-wk diabetic period, however, did not exhibit significantly lower NCV. The mean proportion of the phospholipid fatty acid linoleic acid (18:2n-6) was higher in the sciatic nerves of diabetic rats than in the nondiabetic groups irrespective of dietary lipid treatment. Additionally, the proportion of linoleic acid was higher in the diabetic rats fed sunflower oil than in all other groups. Dietary GLA supplementation did not significantly influence the fatty acid composition of nerve membrane phospholipids and there was no obvious correlation between the fatty acid composition of nerve membrane phospholipids and NCV. The content of fructose and glucose in sciatic nerves was higher, whereas that of myo-inositol was lower, in diabetic rats than in nondiabetic rats; however, this was not significantly influenced by dietary GLA. GLA administration did not significantly influence Na+-K+-exchanging ATPase or ouabain binding activity in sciatic nerve preparations, both of which remained nonsignificantly different in the diabetic and nondiabetic groups. The results suggest that dietary GLA can prevent the deficit in NCV induced by diabetes and that this effect is independent of the nerve phospholipid fatty acid profile, sugar and polyol content, Na+-K+-exchanging ATPase activity, and ouabain binding. GLA may prevent the deficit in NCV indirectly, possibly by its role as a precursor of vasodilatory prostaglandins. These results confirm that GLA is the active component of evening primrose oil.
Key Words: Diabetic neuropathy • streptozotocin • -linolenic acid • nerve conduction velocity • sciatic nerve polyols • Na+-K+-exchanging ATPase • ouabain binding • fatty acids • evening primrose oil • rats
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