Glucose transport and utilization are altered in the brain of rats deficient in n-3 polyunsaturated fatty acids
Version of Record online: 6 JUN 2002
Journal of Neurochemistry
Volume 81, Issue 6, pages 1328–1337, June 2002
How to Cite
Ximenes da Silva, A., Lavialle, F., Gendrot, G., Guesnet, P., Alessandri, J.-M. and Lavialle, M. (2002), Glucose transport and utilization are altered in the brain of rats deficient in n-3 polyunsaturated fatty acids. Journal of Neurochemistry, 81: 1328–1337. doi: 10.1046/j.1471-4159.2002.00932.x
- Issue online: 6 JUN 2002
- Version of Record online: 6 JUN 2002
- Received December 4, 2001; revised manuscript received February 25, 2002; accepted March 13, 2002.
- cytochrome oxidase;
- docosahexaenoic acid;
- energy metabolism;
- glucose transporters;
- glucose uptake;
- polyunsaturated fatty acids
Long-chain polyunsaturated (n-3) fatty acids have been reported to influence the efficiency of membrane receptors, transporters and enzymes. Because the brain is particularly rich in docosahexaenoic acid (DHA, 22:6 n-3), the present study addresses the question of whether the 22:6 n-3 fatty acid deficiency induces disorder in regulation of energy metabolism in the CNS. Three brain regions that share a high rate of energy metabolism were studied: fronto-parietal cortex, hippocampus and suprachiasmatic nucleus. The effect of the diet deficient in n-3 fatty acids resulted in a 30–50% decrease in DHA in membrane phospholipids. Moreover, a 30% decrease in glucose uptake and a 20–40% decrease in cytochrome oxidase activity were observed in the three brain regions. The n-3 deficient diet also altered the immunoreactivity of glucose transporters, namely GLUT1 in endothelial cells and GLUT3 in neurones. In n-3 fatty acid deficient rats, GLUT1-immunoreactivity readily detectable in microvessels became sparse, whereas the number of GLUT3 immunoreactive neurones was increased. However, western blot analysis showed no significant difference in GLUT1 and GLUT3 protein levels between rats deficient in n-3 fatty acids and control rats. The present results suggest that changes in energy metabolism induced by n-3 deficiency could result from functional alteration in glucose transporters.