Essential fatty acid treatment prevents nerve ischaemia and associated conduction anomalies in rats with experimental diabetes mellitus.

In rats with 6 weeks streptozotocin-diabetes there was a 53% reduction in sciatic nerve laser Doppler flux compared to controls (p < 0.01). Treatment of a parallel group of diabetic rats with evening primrose oil, by dietary admixture throughout the protocol, prevented this ischaemia (Doppler flux was 91% of evening primrose-oil-treated controls and was not significantly different). There were no differences in systemic arterial pressure. In another experiment evening primrose oil markedly antagonised the development of exaggerated resistance to anoxic conduction failure in sciatic nerves from diabetic rats. The resistance to anoxia of nerves from non-diabetic rats was also reduced by evening primrose oil. These observations suggest that the sciatic nerves of diabetic rats with short-term streptozotocin-diabetes are markedly ischaemic and that this ischaemia is involved in the development of increased resistance to anoxic/ischaemic conduction failure in diabetic nerve. The findings also promote evening primrose oil as a potential treatment to prevent nerve ischaemia.

The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na+/K+ pump in streptozotocin-diabetic rats.

1. This study examined the effects of dietary essential fatty acid supplementation (5% (w/w) evening primrose oil) upon sciatic motor nerve conduction velocity and 86Rb+ pumping in sciatic nerve endoneurial preparations in rats with 4 to 5 weeks of streptozotocin-induced diabetes. 2. Control diabetic rats (dietary supplementation with 5% (w/w) hydrogenated coconut oil) exhibited a reduction in motor nerve conduction velocity (16%; P less than 0.05) compared to similarly-fed non-diabetic controls, but there was no significant alteration in ouabain-sensitive 86Rb+ pumping, a parameter reflecting activity of the Na+/K+ pump. 3. Treatment of diabetic rats with evening primrose oil prevented completely the development of the motor nerve conduction velocity deficit without affecting the severity of diabetes. Evening primrose oil treatment did not significantly affect motor nerve conduction velocity of non-diabetic animals. 4. Evening primrose oil treatment caused a significant reduction in activity of the Na+/K+ pump in sciatic nerves of diabetic animals (45%; P less than 0.05). 5. These results suggest that the acute conduction velocity defect arising in streptozotocin-diabetic rats, and the actions of evening primrose oil upon this, are independent of any effect on activity of the Na+/K+ pump. Other putative mechanisms are discussed.