| Autor: |
Hsieh, Ya‐Ju, Wu, Liang‐Chih, Ke, Chien‐Chih, Chang, Chi‐Wei, Kuo, Jung‐Wen, Huang, Wen‐Sheng, Chen, Fu‐Du, Yang, Bang‐Hung, Tai, Hsiao‐Ting, Chen, Sharon Chia‐Ju, Liu, Ren‐Shyan |
| Zdroj: |
Alcoholism: Clinical and Experimental Research; February 2018, Vol. 42 Issue: 2 p329-337, 9p |
| Abstrakt: |
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 [1‐11C]‐acetate uptake in the brain. The relationship between the cause and effect of [1‐11C]‐acetate kinetics and acute/chronic EtOH intoxication, however, is still unclear. [1‐11C]‐acetate positron emission tomography (PET) with dynamic measurement of K1and k2rate constants was used to investigate the changes in acetate metabolism in different brain regions of rats with acute or chronic EtOH intoxication. PETimaging demonstrated decreased [1‐11C]‐acetate uptake in rat brain with acute EtOH intoxication, but this increased with chronic EtOH intoxication. Tracer uptake rate constant K1and clearance rate constant k2were decreased in acutely intoxicated rats. No significant change was noted in K1and k2in chronic EtOH intoxication, although 6 of 7 brain regions showed slightly higher k2than 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 PETstudy confirmed the modulatory role of EtOH, administered acutely or chronically, in [1‐11C]‐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. [1‐11C]‐acetate PETimaging is a feasible approach to study the effect of EtOH on acetate metabolism in rat brain. In vivo PET study confirmed the modulatory role of ethanol, administered acutely or chronically, in [1‐11C]‐acetate kinetics and metabolism in the rat brain. Acute ethanol intoxication may inhibit the transport and metabolism of acetate in the brain, whereas chronic ethanol exposure may lead to the adaptation of the rat brain to ethanol in acetate utilisation. [1‐11C]‐Acetate PET imaging is a feasible approach to study the effect of ethanol on acetate metabolism in rat brain. |
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