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 molecul ar species (ACMS) in sciatic nerve phosphatidylcholine and phosphatidy lethanolamine were determined in conjunction with alterations in nerve conduction velocity. Normal and diabetic rats were either untreated o r fed a dietary supplement containing isocalorically equivalent amount s 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 o il treatment. Neither EPO nor corn oil supplementation significantly i ncreased the depressed proportions of ACMS. The level of the linoleoyl -containing molecular species, 16:0/18:2, was elevated in the phosphol ipids from untreated diabetic rats and was further increased by EPO tr eatment. These results are consistent with decreased activity of the D elta 6 desaturase that is required for arachidonic acid synthesis in v ivo, but suggests that an accompanying deficit in the subsequent Delta 5 desaturase-catalyzed reaction may be rate-limiting. These findings indicate that maintenance of normal ACMS levels is not required for pr evention of diminished nerve conduction velocity and suggest that othe r factors influenced by an altered polyunsaturated fatty acid pattern, such as metabolites of linoleic acid or gamma-linolenic acid other th an arachidonic acid, the energy state of the nerve or the degree of me mbrane fluidity may contribute to impaired nerve conduction velocity i n diabetic neuropathy.