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      n-3 Fatty acids modulate brain glucose transport in endothelial cells of the blood-brain barrier.

      Prostaglandins, Leukotrienes, and Essential Fatty Acids
      Animals, Biological Transport, drug effects, Blood-Brain Barrier, cytology, metabolism, Blotting, Western, Cells, Cultured, Docosahexaenoic Acids, pharmacology, Dose-Response Relationship, Drug, Eicosapentaenoic Acid, Endothelial Cells, Fatty Acids, Omega-3, administration & dosage, Fatty Acids, Omega-6, Female, Glucose, pharmacokinetics, Glucose Transporter Type 1, Phosphatidylethanolamines, Pregnancy, Rats

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          Abstract

          We have previously shown that glucose utilization and glucose transport were impaired in the brain of rats made deficient in n-3 polyunsaturated fatty acids (PUFA). The present study examines whether n-3 PUFA affect the expression of glucose transporter GLUT1 and glucose transport activity in the endothelial cells of the blood-brain barrier. GLUT1 expression in the cerebral cortex microvessels of rats fed different amounts of n-3 PUFA (low vs. adequate vs. high) was studied. In parallel, the glucose uptake was measured in primary cultures of rat brain endothelial cells (RBEC) exposed to supplemental long chain n-3 PUFA, docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids, or to arachidonic acid (AA). Western immunoblotting analysis showed that endothelial GLUT1 significantly decreased (-23%) in the n-3 PUFA-deficient microvessels compared to control ones, whereas it increased (+35%) in the microvessels of rats fed the high n-3 PUFA diet. In addition, binding of cytochalasin B indicated that the maximum binding to GLUT1 (Bmax) was reduced in deficient rats. Incubation of RBEC with 15 microM DHA induced the membrane DHA to increase at a level approaching that of cerebral microvessels isolated from rats fed the high n-3 diet. Supplementation of RBEC with DHA or EPA increased the [(3)H]-3-O-methylglucose uptake (reflecting the basal glucose transport) by 35% and 50%, respectively, while AA had no effect. In conclusion, we suggest that n-3 PUFA can modulate the brain glucose transport in endothelial cells of the blood-brain barrier, possibly via changes in GLUT1 protein expression and activity.

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