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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Brain energy metabolism spurns fatty acids as fuel due to their inherent mitotoxicity and potential capacity to unleash neurodegeneration
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Brain energy metabolism spurns fatty acids as fuel due to their inherent mitotoxicity and potential capacity to unleash neurodegeneration

机译：由于其固有的含有尿毒性和潜在的释放神经变性的潜在能力，脑能代谢造成脂肪酸作为燃料

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Abstract The brain uses long-chain fatty acids (LCFAs) to a negligible extent as fuel for the mitochondrial energy generation, in contrast to other tissues that also demand high energy. Besides this generally accepted view, some studies using cultured neural cells or whole brain indicate a moderately active mitochondrial β-oxidation. Here, we corroborate the conclusion that brain mitochondria are unable to oxidize fatty acids. In contrast, the combustion of liver-derived ketone bodies by neural cells is long-known. Furthermore, new insights indicate the use of odd-numbered medium-chain fatty acids as valuable source for maintaining the level of intermediates of the citric acid cycle in brain mitochondria. Non-esterified LCFAs or their activated forms exert a large variety of harmful side-effects on mitochondria, such as enhancing the mitochondrial ROS generation in distinct steps of the β-oxidation and therefore potentially increasing oxidative stress. Hence, the question arises: Why do in brain energy metabolism mitochondria selectively spurn LCFAs as energy source? The most likely answer are the relatively higher content of peroxidation-sensitive polyunsaturated fatty acids and the low antioxidative defense in brain tissue. There are two remarkable peroxisomal defects, one relating to α-oxidation of phytanic acid and the other to uptake of very long-chain fatty acids (VLCFAs) which lead to pathologically high tissue levels of such fatty acids. Both, the accumulation of phytanic acid and that of VLCFAs give an enlightening insight into harmful activities of fatty acids on neural cells, which possibly explain why evolution has prevented brain mitochondria from the equipment with significant β-oxidation enzymatic capacity. Highlights ? Cerebral mitochondria use fatty acids to a negligible extent for energy generation. ? High fatty acid levels at defective peroxisomes uncover fatty acids’ mitotoxicity. ? Fatty acid burning in non-cerebral mitochondria is linked to high ROS generation. ? Brain dislikes fatty acids as fuel due to its high peroxidation sensitivity. ? Refsum disease and X-linked adrenoleukodystrophy are due to peroxisomal defects.
机译：摘要大脑使用长链脂肪酸（LCFA）在对线粒体能量产生的燃料中可以忽略不计的程度，与其他也需要高能量的其他组织。除了这普遍接受的视图之外，还使用培养的神经细胞或全脑的一些研究表明了中度活性的线粒体β-氧化。在这里，我们证实了脑线粒体无法氧化脂肪酸的结论。相反，神经细胞通过神经细胞燃烧肝脏衍生的酮体是众所周知的。此外，新的见解表明，使用奇数中链脂肪酸作为维持脑线粒体中柠檬酸循环的中间体水平的有价值的源。非酯化的LCFA或其活化的形式对线粒体产生大量有害的副作用，例如增强β-氧化的不同步骤中的线粒体ROS，因此可能增加氧化应激。因此，问题出现了：为什么脑能量代谢线粒体有选择地将LCFA作为能源？最可能的答案是过氧化敏感的多不饱和脂肪酸的含量相对较高，脑组织中的低抗氧化防御。存在两种显着的过氧杀菌缺陷，与植物酸的α-氧化有关，另一个是对非常长的链链脂肪酸（VLCFA）的吸收，这导致这种脂肪酸的病于病理上高的组织水平。两者，植物酸的积累以及VLCFA的积累，对神经细胞的脂肪酸的有害活性提出了启发性的洞察力，这可能解释了为什么进化从具有显着β-氧化酶活性的设备中预防脑线粒体。强调 ？脑线粒体使用脂肪酸在能量产生的可忽略范围内。还过氧化血剂缺陷的高脂肪酸水平揭示脂肪酸的乳腺毒性。还在非脑线粒体中燃烧的脂肪酸与高ROS产生联系。还由于其高过氧化敏感性，大脑不喜欢脂肪酸作为燃料。还Refsum疾病和X-连接的肾上腺胁迫张力学是由于过氧缺项缺陷。

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