(n-3) polyunsaturated fatty acid deficiency reduces the expression of both isoforms of the brain glucose transporter GLUT1 in rats.
Level 5 - mechanism / opinion, no new human data
Animal experimental study
PubMed 16140905 · doi:10.1093/jn/135.9.2241
What was done
Adult male rats (first generation) were fed either a diet lacking (n-3) polyunsaturated fatty acids or a control diet. Researchers quantified fatty acid compositions in phospholipid fractions of isolated cerebral cortex microvessels and homogenates. They measured protein expression of the 55-kDa (blood-brain barrier) and 45-kDa (astrocyte) GLUT1 isoforms and neuronal GLUT3 by Western blotting, and assessed GLUT1 mRNA levels using real-time RT-PCR.
What was found
Microvessels and cortex homogenates of rats on the deficient diet had 50% lower docosahexaenoic acid [22:6(n-3)] levels relative to controls, with 22:6(n-3) replaced by 22:5(n-6). Protein expression of 55-kDa GLUT1 in microvessels decreased by 25% (P < 0.01) and 45-kDa GLUT1 in cortex homogenates decreased by 30% (P < 0.01). GLUT3 protein expression and GLUT1 mRNA levels did not significantly change.
Why it matters
This study demonstrates that omega-3 deficiency impairs brain glucose transporter expression at the post-transcriptional level, identifying a specific biochemical mechanism for reduced cerebral glucose utilization.
Limits
The study was conducted entirely in an animal model (rats) and may not translate to humans. Exact sample sizes (n) were not reported in the abstract. Functional in vivo glucose transport rates were not directly measured.
Cited by
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