Abstract
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.
Highlights
Introduction andRadiobiology, Universite de Sherbrooke, Among nutrients improving human health, n-3 polyunsaturated fatty acids (n-3 PUFA) have received wide attention during the last two decades
Article received 11 May 2012 Accepted 22 May 2012 deficiency which led us to hypothesize that Docosahexaenoic acid (DHA) brain concentration could regulate neuronal activity by controlling brain energy metabolism and glucose utilization and transport (Ximenes et al, 2002)
It is first transported across the endothelial cells of the blood-brain barrier (BBB) by the 55-kDa GLUT1 localized at the luminal and abluminal sides of the cells, into astrocytes by the 45-kDa GLUT1 isoform and into neurons by GLUT3 (Duelli and Kuschinsky, 2001)
Summary
The brain represents only 2% of the body mass, it consumes about 25% of glucose and 20% oxygen used by the body. The reversion of Na+ and K+ fluxes across the cell membrane consumes about 80% of brain ATP by requiring the activation of the neuronal Na+/K+ ATPase coupled to the inversion of ion fluxes against their concentration gradient. Glucose is distributed from the blood to the brain cells via specific membrane glucose transporters (GLUTs), mainly GLUT1 and GLUT3 It is first transported across the endothelial cells of the blood-brain barrier (BBB) by the 55-kDa GLUT1 localized at the luminal (facing the blood) and abluminal (facing the parenchyma) sides of the cells, into astrocytes by the 45-kDa GLUT1 isoform and into neurons by GLUT3 (Duelli and Kuschinsky, 2001) (figure 1). The activation of a brain area involved in memory processing, the hippocampus, increases GLUT1 gene and protein expressions of both endothelial and astrocytic isoforms (Choeiri et al, 2005). The expression of neuronal GLUT3 does not change, supporting the concept
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