EVENING PRIMROSE OIL TREATMENT CORRECTS REDUCED CONDUCTION-VELOCITY BUT NOT DEPLETION OF ARACHIDONIC-ACID IN NERVE FROM STREPTOZOTOCIN-INDUCED DIABETIC RATS
R. Kuruvilla et al., EVENING PRIMROSE OIL TREATMENT CORRECTS REDUCED CONDUCTION-VELOCITY BUT NOT DEPLETION OF ARACHIDONIC-ACID IN NERVE FROM STREPTOZOTOCIN-INDUCED DIABETIC RATS, Prostaglandins, leukotrienes and essential fatty acids, 59(3), 1998, pp. 195-202
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.