ACCELERATION OF EXPERIMENTAL DIABETIC-RETINOPATHY IN THE RAT BY OMEGA-3-FATTY-ACIDS

Omega-3 fatty acids exert several important biological effects on fact ors that may predispose to diabetic retinopathy. Potential pathogeneti c mechanisms include platelet dysfunction, altered eicosanoid producti on, increased blood viscosity in association with impaired cell deform ability and pathologic leucocyte/endothelium interaction. Therefore, w e tested whether a 6-month administration of fish oil (750 mg Maxepa, 5 times per week), containing 14% eicosapentaenoic acid (EPA) and 10% docosahexaenic acid, could inhibit the development of experimental ret inopathy of the streptozotocin-diabetic rat. The efficiency of fish oi l supplementation was evaluated by measuring EPA concentrations in tot al, plasma and membrane fatty acids and by measuring the generation of lipid mediators (leukotrienes and thromboxanes). Retinal digest prepa rations were quantitatively analysed for pericyte loss, and the format ion of acellular capillaries. Omega-3 fatty acid administration to dia betic rats resulted in a twofold increase of EPA 20:5 in total fatty a cids, and a reduction of the thromboxane(2/3) ratio from 600 (untreate d diabetic rats) to 50 (treated diabetic rats). Despite these biochemi cal changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75% in the fish oil treated diabetic group (115.1 +/- 26.8; untreated dia betic 65.2 +/- 15.0 acellular capillary segments/mm(2) of retinal area ). We conclude from this study that dietary fish oil supplementation m ay be harmful for the diabetic microvasculature in the retina.