Insights into the metabolic response to traumatic brain injury as revealed by (13)C NMR spectroscopy.
Insights into the metabolic response to traumatic brain injury as revealed by (13)C NMR spectroscopy.
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DOI：
10.3389/fnene.2013.00008
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发表时间：
2013-10-04
期刊：
影响因子：
--
通讯作者：
Sutton RL
中科院分区：
文献类型：
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作者：
Bartnik-Olson BL;Harris NG;Shijo K;Sutton RL
本综述强调了创伤性脑损伤（TBI）后脑代谢相关的关键问题，以及使用13 C标记底物和核磁共振（NMR）光谱来研究这些变化。首先，我们解决一些病理生理因素，导致代谢功能障碍后TBI。然后，我们研究了如何使用13 C NMR光谱策略来研究损伤后的能量代谢、神经传递、细胞内氧化还原状态和神经胶质细胞区室化。脑提取物的13 C NMR光谱研究TBI的动物模型已经揭示了乳酸的糖酵解产生增强，戊糖磷酸途径（PPP）激活的证据，以及依赖于损伤严重程度的神经元和星形胶质细胞氧化代谢的改变。从13 C标记的葡萄糖或乙酸盐到谷氨酸盐和谷氨酰胺中的标记的差异掺入也表明TBI诱导的对谷氨酸盐-谷氨酰胺循环的适应。
The present review highlights critical issues related to cerebral metabolism following traumatic brain injury (TBI) and the use of 13C labeled substrates and nuclear magnetic resonance (NMR) spectroscopy to study these changes. First we address some pathophysiologic factors contributing to metabolic dysfunction following TBI. We then examine how 13C NMR spectroscopy strategies have been used to investigate energy metabolism, neurotransmission, the intracellular redox state, and neuroglial compartmentation following injury. 13C NMR spectroscopy studies of brain extracts from animal models of TBI have revealed enhanced glycolytic production of lactate, evidence of pentose phosphate pathway (PPP) activation, and alterations in neuronal and astrocyte oxidative metabolism that are dependent on injury severity. Differential incorporation of label into glutamate and glutamine from 13C labeled glucose or acetate also suggest TBI-induced adaptations to the glutamate-glutamine cycle.