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A more recent version of this article appeared on January 1, 2008
Papers In Press, published online ahead of print October 11, 2007
J. Lipid Res., doi:10.1194/jlr.M700386-JLR200
Submitted on August 27, 2007
Revised on October 10, 2007
Accepted on October 11, 2007
The low-density lipoprotein receptor is not necessary for maintaining mouse brain polyunsaturated fatty acid concentrations
Chuck T. Chen, Dawid W. L. Ma, John H. Kim, Howard T. J. Mount, and Richard P. Bazinet
Nutritional Sciences, University of Toronto, Toronto, ON M5S 3E2
Corresponding Author: richard.bazinet{at}utoronto.ca
The brain cannot synthesize n-6 or n-3 polyunsaturated fatty acids (PUFA) de novo and requires their transport from the blood. Two models of brain fatty acid uptake have been proposed. One requires the passive diffusion of unesterified fatty acids through endothelial cells of the blood-brain barrier and the other model requires the uptake of lipoproteins via a lipoprotein receptor on the luminal membrane of endothelial cells. This study tested if the low-density lipoprotein receptor (LDLr) is necessary for maintaining brain PUFA concentrations. Because the cortex has a low basal expression of LDLr while the anterior brain stem has a relatively high expression, we analyzed these regions separately. LDLr-/- and wildtype mice consumed an AIN-93G diet ad libitum until 7 weeks of age. After microwaving, the cortex and anterior brain stem (pons and medulla) were isolated for phospholipid fatty acid analyses. There were no differences in phosphatidylserine, phosphatidylinositol, ethanolamine or choline glycerophospholipid esterified PUFA, saturated or monounsaturated fatty acid concentrations in the cortex or brain stem between LDLr-/- and wildtype mice. The findings demonstrate that the LDLr is not necessary for maintaining brain PUFA concentrations and suggest that other mechanisms to transport PUFA into the brain must exist.

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Copyright © 2007 by the American Society for Biochemistry and Molecular Biology.
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