Why glucose transport in the brain matters for PET
Why glucose transport in the brain matters for PET
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DOI：
10.1016/j.tins.2005.01.002
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发表时间：
2005-03-01
影响因子：
15.9
通讯作者：
Bittner, CX
中科院分区：
文献类型：
--
作者：
Barros, LF;Porras, OH;Bittner, CX
神经元活动由葡萄糖代谢提供动力，葡萄糖代谢是基础研究和使用氟脱氧葡萄糖正电子发射断层扫描（FDG-PET）进行临床诊断的一种现象。根据目前的观点，葡萄糖转运到大脑中不是限速的;因此，它不能控制新陈代谢。这篇文章通过显示基础转运徘徊在其最大值附近，使得代谢活化不能自行增加通量来挑战这种观点。鉴于最近关于优先分解葡萄糖的细胞类型的证据，我们认为FDG-PET报告了星形胶质细胞而不是神经元中葡萄糖转运和代谢的协同激活。
Neuronal activity is fueled by glucose metabolism, a phenomenon exploited in basic research and clinical diagnosis using fluorodeoxyglucose positron emission tomography (FDG-PET). According to the current view, glucose transport into the brain is not rate-limiting; thus, it cannot exert control over metabolism. This article challenges such a view by showing that basal transport hovers near its maximum, making metabolic activation unable to increase flux on its own. In the light of recent evidence on the identity of the cell type that preferentially breaks down glucose, we suggest that FDG-PET reports the synergistic activation of glucose transport and metabolism in astrocytes, rather than in neurons.