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CD36的基因消融不会改变小鼠脑内多不饱和脂肪酸的浓度。

Genetic ablation of CD36 does not alter mouse brain polyunsaturated fatty acid concentrations.

作者信息

Song Byung Jun, Elbert Adrienne, Rahman Tupur, Orr Sarah K, Chen Chuck T, Febbraio Maria, Bazinet Richard P

机构信息

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, FitzGerald Building, 150 College St., Room 306, Toronto, ON M5S3E2, Canada.

出版信息

Lipids. 2010 Apr;45(4):291-9. doi: 10.1007/s11745-010-3398-z. Epub 2010 Mar 20.

DOI:10.1007/s11745-010-3398-z
PMID:20306148
Abstract

In the brain, polyunsaturated fatty acids (PUFA), especially arachidonic acid and docosahexaenoic acid (DHA), are required for regulating membrane fluidity, neuronal survival and signal transduction. Since the brain cannot synthesize n-6 and n-3 PUFA de novo, they must be supplied from the blood. However, the methods of PUFA entry into the brain are not agreed upon. This study tested the necessity of CD36, a candidate transporter of unesterified fatty acids, for maintaining brain PUFA concentrations by comparing brain PUFA concentrations in CD36(-/-) mice to their wild-type littermates. Because CD36(-/-) mice have been reported to have impaired learning ability, the PUFA concentrations in different brain regions (cortex, hippocampus, cerebellum and the remainder of brain) were investigated. At 9 weeks of age, the brain was separated into the four regions and fatty acid concentrations in total and phospholipid classes of these brain regions were analyzed using thin layer and gas chromatography. There were no statistical differences in arachidonic acid or DHA concentrations in the different brain regions between wild-type and CD36(-/-) mice, in total or phospholipid fractions. Concentrations of monounsaturated fatty acids were decreased in several phospholipid fractions in CD36(-/-) mice. These findings suggest that CD36 is not necessary for maintaining brain PUFA concentrations and that other mechanisms must exist.

摘要

在大脑中,多不饱和脂肪酸(PUFA),尤其是花生四烯酸和二十二碳六烯酸(DHA),对于调节膜流动性、神经元存活和信号转导是必需的。由于大脑无法从头合成n-6和n-3多不饱和脂肪酸,它们必须从血液中获取。然而,多不饱和脂肪酸进入大脑的方式尚无定论。本研究通过比较CD36基因敲除(CD36(-/-))小鼠与其野生型同窝小鼠大脑中的多不饱和脂肪酸浓度,来测试未酯化脂肪酸的候选转运体CD36对于维持大脑多不饱和脂肪酸浓度的必要性。由于已有报道称CD36(-/-)小鼠的学习能力受损,因此对不同脑区(皮层、海马体、小脑和大脑其余部分)的多不饱和脂肪酸浓度进行了研究。在9周龄时,将大脑分离为这四个区域,并使用薄层色谱法和气相色谱法分析这些脑区中总脂肪酸和磷脂类别的脂肪酸浓度。在野生型和CD36(-/-)小鼠的不同脑区中,花生四烯酸或DHA的总浓度或磷脂部分浓度均无统计学差异。CD36(-/-)小鼠的几个磷脂部分中,单不饱和脂肪酸的浓度降低。这些发现表明,CD36对于维持大脑多不饱和脂肪酸浓度并非必需,必然存在其他机制。

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Prostaglandins Leukot Essent Fatty Acids. 2010 Feb-Mar;82(2-3):141-5. doi: 10.1016/j.plefa.2009.11.003. Epub 2010 Jan 27.
2
Effects of dietary docosahexaenoic acid connecting phospholipids on the learning ability and fatty acid composition of the brain.膳食二十二碳六烯酸连接磷脂对大脑学习能力和脂肪酸组成的影响。
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3
Brain phospholipid arachidonic acid half-lives are not altered following 15 weeks of N-3 polyunsaturated fatty acid adequate or deprived diet.
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Eur J Neurosci. 2021 Apr;53(8):2500-2510. doi: 10.1111/ejn.15147. Epub 2021 Feb 28.
4
Neuronal Lipoprotein Lipase Deficiency Alters Neuronal Function and Hepatic Metabolism.神经元脂蛋白脂肪酶缺乏会改变神经元功能和肝脏代谢。
Metabolites. 2020 Sep 28;10(10):385. doi: 10.3390/metabo10100385.
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