Evening primrose oil treatment corrects reduced conduction velocity but not depletion of arachidonic acid in nerve from streptozotocin-induced diabetic rats.

The effects of evening primrose oil (EPO) treatment, a source of gamma-linolenic acid, on the proportions of arachidonoyl-containing molecular species (ACMS) in sciatic nerve phosphatidylcholine and phosphatidylethanolamine were determined in conjunction with alterations in nerve conduction velocity. Normal and diabetic rats were either untreated or fed a dietary supplement containing isocalorically equivalent amounts of either EPO or corn oil for the duration of the experiment. After 8 weeks of streptozotocin-induced diabetes, nerve conduction velocity was reduced 16% and this deficit was prevented by either EPO or corn oil treatment. Neither EPO nor corn oil supplementation significantly increased the depressed proportions of ACMS. The level of the linoleoyl-containing molecular species, 16:0/18:2, was elevated in the phospholipids from untreated diabetic rats and was further increased by EPO treatment. These results are consistent with decreased activity of the delta6 desaturase that is required for arachidonic acid synthesis in vivo, but suggests that an accompanying deficit in the subsequent delta5 desaturase-catalyzed reaction may be rate-limiting. These findings indicate that maintenance of normal ACMS levels is not required for prevention of diminished nerve conduction velocity and suggest that other factors influenced by an altered polyunsaturated fatty acid pattern, such as metabolites of linoleic acid or gamma-linolenic acid other than arachidonic acid, the energy state of the nerve or the degree of membrane fluidity may contribute to impaired nerve conduction velocity in diabetic neuropathy.