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

Abstract

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 < 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 < 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.

Interactions between essential fatty acid, prostanoid, polyol pathway and nitric oxide mechanisms in the neurovascular deficit of diabetic rats

“…Thus, the vascular effects of EPO and ARI treatments can be identified with increased prostacyclin and NO action respectively, although this may be an oversimplification since ARI treatment partially corrected reduced aorta prostacyclin output [29] and a deficit in the pressor response to arachidonic acid [30] in diabetic rats. No effects of EPO on polyol pathway metabolites were observed, in agreement with previous findings [31,32].…”

“…Taken together, these data suggest that a myo-inositol/Na-K ATPase mechanism is unlikely to contribute to the NCV or blood flow results. Furthermore, NCV deficits are corrected by vasodilator or EPO treatments that do not alter Na-K ATPase activity [32,39] and ARI/myo-inositol effects on Na-K ATPase are only found in rats fed a high sucrose diet [4O].…”

Effects of anti-oxidant treatment on sciatic nerve dysfunction in streptozotocin-diabetic rats; comparison with essential fatty acids

“…We have previously shown that the reduced sciatic nerve laser Doppler flux in diabetic rats indicates possible ischaemia and that a high dose of evening primrose oil has the potential to prevent nerve ischaemia and conduction abnormalities [5,40]. We also reported that evening primrose oil treatment increases tissue prostacyclin production [9].…”

Acetylcholine‐induced arteriolar dilation is reduced in streptozotocin‐induced diabetic rats with motor nerve dysfunction

“…In other studies, pathways involving the metabolism of arachidonic acid could also be involved in mediating changes in vascular reactivity. Supplementing diabetic rats with γ‐linolenic acid, an arachidonic acid precursor, has been shown to improve motor nerve conduction velocity and neuronal blood flow in the sciatic nerve (Lockett & Tomlinson, 1992; Karasu et al ., 1995; Cameron et al ., 1996; Cotter & Cameron, 1997). Furthermore, the prostacyclin analogue beraprost sodium has been shown to increase sciatic nerve blood flow in diabetic rats (Hotta et al ., 1996).…”