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The very low density lipoprotein receptor is not necessary for maintaining brain polyunsaturated fatty acid concentrations
Authors:Tupur Rahman  Ameer Y. Taha  Byung Jun Song  Sarah K. Orr  Zhen Liu  Chuck T. Chen  Richard P. Bazinet
Affiliation:1. State Key Laboratory of Organic Geochemistry, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou 510640, China;2. National Institute for Agro-Environmental Sciences, Tsukuba, Ibaraki 305-8604, Japan;3. Certification and Business Team, Foundation of Ag. Tech Commercialization and Transfer (FACT), 211-2 Seodun-dong Gwonseon-gu, Suwon 441-857, Republic of Korea;4. Lancaster Environment Centre, Lancaster University, Lancaster LA1 4YQ, UK
Abstract:
Polyunsaturated fatty acids (PUFA), especially docosahexaenoic and arachidonic acids, as well as cholesterol are important for neural development and maintaining brain function. However, in contrast to cholesterol, the brain is unable to synthesize the required amounts of these PUFA de novo and requires a constant supply from plasma. Suggested pools of uptake include plasma unesterified PUFA or the uptake of PUFA-containing lipoproteins via lipoprotein receptors into endothelial cells of the blood brain barrier. Our study tested whether the very low density lipoprotein receptor (VLDLr) is necessary for maintaining brain PUFA and cholesterol concentrations. Moreover, since VLDLr knockout (VLDLr?/?) mice have been reported to have behavioural deficits, this study asked the question whether altered brain PUFA and cholesterol concentrations might be related to these deficits. VLDLr?/? and wild-type mice had ad libitum access to chow. At 7 weeks of age the mice were sacrificed, and the cortex, cerebellum, hippocampus, and the remainder of the brain were isolated for total fatty acid and cholesterol analyses. There were no differences in total lipid PUFA or cholesterol concentrations in any of the four brain regions between VLDLr?/? and wild-type mice. These findings demonstrate that the VLDLr 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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