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A deficiency in essential fatty acid metabolism has been widely reported in both human and animal diabetes. Fish oil supplementations (n-3 fatty acids), containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), were less effective on diabetic neuropathy than (n-6) fatty acids. This partial effect of (n-3) fatty acids might be attributed to the presence of EPA, a competitor of arachidonic acid, which enhanced the diabetes-induced decrease of this fatty acid in serum and tissues. For determining whether a supplementation with DHA alone could prevent neuropathy in streptozotocin-induced diabetes, diabetic rats were given daily, by gavage, liposomes containing DHA phospholipids, at a dose of 60 mg/kg. Eight weeks of diabetes induced significant decreases in nerve conduction velocity (NCV), nerve blood flow (NBF), and sciatic nerve and erythrocyte (red blood cells [RBCs]) Na,K-ATPase activities. DHA phospholipids totally prevented the decrease in NCV and NBF observed during diabetes when compared with the nonsupplemented diabetic group. DHA phospholipids also prevented the Na,K-ATPase activity decrease in RBC but not in sciatic nerve. Moreover, DHA level in sciatic nerve membranes was correlated with NCV. These results demonstrate a protective effect of daily doses of DHA on experimental diabetic neuropathy. Thus, treatment with DHA phospholipids could be suitable for evaluation in clinical trials. Diabetes 52:2578-2585, 2003
AA, arachidonic acid; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; GLA, [gamma]-linolenic acid; LA, linoleic acid; MUFA, monounsaturated fatty acid; NBF, nerve blood flow; NCV, nerve conduction velocity; P^sub i^, inorganic phosphate; PPAR, peroxisome proliferator-activated receptor; PUFA, polyunsaturated fatty acid; RBC, red blood cell; SFA, saturated fatty acid; STZ, streptozotocin.
(C) 2003 by the American Diabetes Association.
In type 1 diabetes, hyperglycemia and hypoinsulinemia lead to a spectrum of metabolic and vascular abnormalities, including an increase of the polyol pathway, abnormalities in lipid metabolism, advanced glycosylated end product formation, increased oxidative damage, defects in growth factors, and endoneurial hypoxia (1,2). Although the cause of diabetic neuropathy remains unknown, its correlation with these aforementioned changes seems to occur in a similar temporal sequence (3). Diabetes impairs essential fatty acid metabolism by decreasing activities of [Delta]6 and [Delta]5 desaturases, enzymes that convert dietary linoleic acid (LA) and [alpha]-linolenic acid to long-chain polyunsaturated fatty acids (PUFA), including [gamma]-linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid...