(n-3) Polyunsaturated Fatty Acid Deficiency Reduces the Expression of Both Isoforms of the Brain Glucose Transporter GLUT1 in Rats
The Journal of Nutrition. 2005-09-01; 135(9): 2241-2246
DOI: 10.1093/jn/135.9.2241
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Pifferi F(1), Roux F, Langelier B, Alessandri JM, Vancassel S, Jouin M, Lavialle M, Guesnet P.
Author information:
(1)Nutrition and Food Safety Laboratory Unit, Neurobiology of Lipids, Institut
National de la Recherche Agronomique (INRA), Jouy-en-Josas, 78352 Cedex, France.
The altered neuron activity of rats deficient in (n-3) PUFAs may be due in part
to a decrease in brain glucose utilization and glucose transport. We measured
the glucose transporter protein GLUT1 isoforms at the blood-brain barrier
(55-kDa) and in astrocytes (45-kDa) by Western immunoblotting and their mRNA by
real time RT-PCR analysis in the cerebral cortex of adult male rats fed diets
lacking (n-3) fatty acids (1st generation). The neuron glucose transporter GLUT3
was also assayed. The fatty acids in the phosphatidylcholine (PC), ethanolamine
phosphoglycerolipid (EPG), and phosphatidylserine (PS) fractions of isolated
microvessels and homogenates of the cerebral cortex were determined. The levels
of (n-6) PUFAs [mainly arachidonic acid, 20:4(n-6)] in the phospholipid
fractions of microvessels were higher and the levels of (n-3) PUFAs [mainly
docosahexaenoic acid, 22:6(n-3)] were lower than in cerebral cortex homogenates.
The microvessels and cortex of rats fed the (n-3) PUFA-deficient diet had 50% of
the control 22:6(n-3) contents; 22:6(n-3) was replaced by 22:5(n-6). The 55-kDa
GLUT1 immunoreactivity in (n-3) PUFA-deficient microvessels was decreased (down
25%, P < 0.01), as was the 45 kDa-GLUT1 in the homogenate (down 30%, P < 0.01).
But the amount of immunoreactivity of GLUT3 did not change. The amount of GLUT1
mRNA was not affected by the (n-3) PUFA-deficient diet. These results suggest
that the decreased glucose utilization in the cerebral cortex of (n-3)
PUFA-deficient rats is due to reduced amounts of the 2 isoforms of GLUT1,
indicating post-transcriptional regulation of GLUT1 synthesis.