Volume 19, Number 4, Juillet-Août 2012
|Page(s)||238 - 244|
|Published online||15 July 2012|
N-3 fatty acids, neuronal activity and energy metabolism in the brain
NuRéLiCe, INRA, Jouy-en-Josas, France
2 Mécanismes Adaptatifs et Evolution, UMR 7179 CNRS, Muséum National d’Histoire Naturelle, Brunoy, France
3 Research Center on Aging and Department of Medicine, Université de Sherbrooke, Sherbrooke, QC, Canada
4 Departement of Nuclear Medecine and Radiobiology, Université de Sherbrooke, Sherbrooke, QC, Canada
5 Lesieur, 29 quai Aulagnier, Asnières sur Seine, France
6 PG Consulting, 13 villa Bellevue, Bures sur Yvette, France
Accepted: 22 May 2012
The content of docosahexaenoic acid (DHA) in brain membranes is of crucial importance for the optimum development of brain functions. A lack of DHA accretion in the brain is accompanied by deficits in learning behavior linked to impairments in neurotransmission processes, which might result from alteration of brain fuel supply and hence energy metabolism. Experimental data we published support the hypothesis that n-3 fatty acids may modulate brain glucose utilization and metabolism. Indeed rats made deficient in DHA by severe depletion of total n-3 fatty acid intake have 1) a lower brain glucose utilization, 2) a decrease of the glucose transporter protein content GLUT1 both in endothelial cells and in astrocytes, 3) a repression of GLUT1 gene expression in basal state as well as upon neuronal activation. This could be due to the specific action of DHA on the regulation of GLUT1 expression since rat brain endothelial cells cultured with physiological doses of DHA had an increased GLUT1 protein content and glucose transport when compared to non-supplemented cells. These experimental data highlight the impact of n-3 fatty acids on the use of brain glucose, thereby constituting a key factor in the control of synaptic activity. This emerging role suggests that dietary intake of n-3 fatty acids can help to reduce the cognitive deficits in the elderly and possibly symptomatic cerebral metabolic alterations in Alzheimer disease by promoting brain glucose metabolism.
Key words: Ageing / Alzheimer / Brain / Glucose metabolism / Glucose transporter GLUT1 / Docosahexaenoic acid (DHA) / N-3 fatty acids
© John Libbey Eurotext 2012
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