Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Stress. 2011 Jan;14(1):66-72. doi: 10.3109/10253890.2010.506931. Epub 2010 Oct 11.
Associations between uncoupling protein (UCP) expression and functional changes in myocardial mitochondrial bio-energetics have not been well studied during periods of starvation stress. Our aim was to study the effects of acute starvation, for 24 or 48 h, on combined cardiac mitochondrial function and UCP expression in mice. Isolated heart mitochondria from female mice starved for 48 h compared to that from mice fed revealed a significantly (p < 0.05) decreased adenosine diphosphate-to-oxygen ratio, a significantly increased proton leak and an increased GTP inhibition on palmitic acid-induced state 4 oxygen consumption (p < 0.05). These bio-energetic functional changes were associated with increases in mitochondrial UCP2 and UCP3 protein expression. In conclusion, our findings suggest that increased UCP2 and UCP3 levels may contribute to decreased myocardial mitochondrial bio-energetic function due to starvation.
在饥饿应激期间，解偶联蛋白（UCP）表达与心肌线粒体生物能量学功能变化之间的关系尚未得到很好的研究。我们的目的是研究急性饥饿（24 或 48 小时）对饥饿 48 小时的雌性小鼠和正常饮食的小鼠的心脏线粒体功能和 UCP 表达的影响。与正常饮食的小鼠相比，饥饿 48 小时的小鼠心脏线粒体的三磷酸腺苷到氧的比值显著降低（p < 0.05），质子漏显著增加，GTP 对棕榈酸诱导的状态 4 耗氧量的抑制作用增加（p < 0.05）。这些生物能量功能变化与线粒体 UCP2 和 UCP3 蛋白表达的增加有关。总之，我们的研究结果表明，由于饥饿，UCP2 和 UCP3 水平的增加可能导致心肌线粒体生物能量功能降低。
