Department of Medical Imaging and Radiological Sciences, Kaohsiung Medical University, Kaohsiung, Taiwan.
Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Alcohol Clin Exp Res. 2018 Feb;42(2):329-337. doi: 10.1111/acer.13573. Epub 2018 Jan 22.
Ethanol (EtOH) intoxication inhibits glucose transport and decreases overall brain glucose metabolism; however, humans with long-term EtOH consumption were found to have a significant increase in [1- C]-acetate uptake in the brain. The relationship between the cause and effect of [1- C]-acetate kinetics and acute/chronic EtOH intoxication, however, is still unclear.
[1- C]-acetate positron emission tomography (PET) with dynamic measurement of K and k rate constants was used to investigate the changes in acetate metabolism in different brain regions of rats with acute or chronic EtOH intoxication.
PET imaging demonstrated decreased [1- C]-acetate uptake in rat brain with acute EtOH intoxication, but this increased with chronic EtOH intoxication. Tracer uptake rate constant K and clearance rate constant k were decreased in acutely intoxicated rats. No significant change was noted in K and k in chronic EtOH intoxication, although 6 of 7 brain regions showed slightly higher k than baseline. These results indicate that acute EtOH intoxication accelerated acetate transport and metabolism in the rat brain, whereas chronic EtOH intoxication status showed no significant effect.
In vivo PET study confirmed the modulatory role of EtOH, administered acutely or chronically, in [1- C]-acetate kinetics and metabolism in the rat brain. Acute EtOH intoxication may inhibit the transport and metabolism of acetate in the brain, whereas chronic EtOH exposure may lead to the adaptation of the rat brain to EtOH in acetate utilization. [1- C]-acetate PET imaging is a feasible approach to study the effect of EtOH on acetate metabolism in rat brain.
乙醇（EtOH）中毒会抑制葡萄糖转运并降低整体脑葡萄糖代谢；然而，长期摄入乙醇的人类被发现大脑中[1- C]-乙酸摄取量显著增加。然而，[1- C]-乙酸动力学与急性/慢性乙醇中毒之间的因果关系仍不清楚。
使用[1- C]-乙酸正电子发射断层扫描（PET）进行动态测量 K 和 k 速率常数，以研究急性或慢性乙醇中毒大鼠不同脑区乙酸代谢的变化。
PET 成像显示急性乙醇中毒大鼠大脑中[1- C]-乙酸摄取减少，但慢性乙醇中毒大鼠中乙酸摄取增加。急性中毒大鼠的示踪剂摄取率常数 K 和清除率常数 k 降低。慢性乙醇中毒时 K 和 k 没有明显变化，尽管 7 个脑区中有 6 个的 k 值略高于基线。这些结果表明，急性乙醇中毒加速了大鼠大脑中乙酸的转运和代谢，而慢性乙醇中毒状态则没有明显影响。
体内 PET 研究证实，急性或慢性给予乙醇对大鼠大脑中[1- C]-乙酸动力学和代谢具有调节作用。急性乙醇中毒可能抑制大脑中乙酸的转运和代谢，而慢性乙醇暴露可能导致大鼠大脑对乙酸利用中乙醇的适应。[1- C]-乙酸 PET 成像可能是研究乙醇对大鼠大脑中乙酸代谢影响的一种可行方法。
