Ethanol alters lipid profiles and phosphorylation status of AMP-activated protein kinase in the neonatal mouse brain.
Ethanol alters lipid profiles and phosphorylation status of AMP-activated protein kinase in the neonatal mouse brain.
复制标题
乙醇改变新生小鼠大脑中的脂质谱和 AMP 激活蛋白激酶的磷酸化状态。
DOI：
10.1111/j.1471-4159.2007.04836.x
复制
发表时间：
2007
影响因子：
4.7
通讯作者：
Saito,Mitsuo
中科院分区：
文献类型：
--
作者：
Saito,Mariko;Chakraborty,Goutam;Mao,Rui-Fen;Wang,Ray;Cooper,ThomasB;Vadasz,Csaba;Saito,Mitsuo
Previously, we have shown that ethanol‐induced apoptosis in cultured neurons is accompanied by changes in cellular lipid profiles. In the present study, the effects of ethanol on brain lipid metabolism were studied using 7‐day‐old C57BL/6ByJ mice, which display apoptotic neurodegeneration upon exposure to ethanol. The brain lipids were extracted 4–24 h after the ethanol or saline treatment, and analyzed by TLC. We found that the levels of triglyceride, cholesterol ester, ceramide, andN‐acylphosphatidylethanolamine increased significantly in the brains of ethanol‐treated mice compared to those of saline‐treated mice. Concomitantly, ethanol reduced Thr172 phosphorylation of AMP‐activated protein kinase (AMPK) α subunits. Ethanol also reduced phosphorylation of acetyl‐CoA carboxylase, a substrate of AMPK and a lipogenic enzyme known to be activated by dephosphorylation. In contrast, lipid profiles of 19‐day‐old mouse brains, which scarcely manifested neurodegeneration upon ethanol exposure, were not significantly affected by ethanol. Also, the basal levels of Thr172‐phosphorylated AMPK α were lower in these brains than in 7‐day‐old mouse brains, and no detectable changes in the phosphorylation status were observed by ethanol treatment. Our findings indicate that the ethanol‐induced apoptotic neurodegeneration observed in mice during restricted developmental periods is accompanied by alterations in both the lipid content and the activity of AMPK in the brain.
