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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Acetate supplementation increases brain phosphocreatine and reduces AMP levels with no effect on mitochondrial biogenesis
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Acetate supplementation increases brain phosphocreatine and reduces AMP levels with no effect on mitochondrial biogenesis

机译：补充醋酸盐可增加脑磷酸肌酸并降低AMP水平，而不会影响线粒体的生物发生

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Acetate supplementation in rats increases plasma acetate and brain acetyl-CoA levels. Although acetate is used as a marker to study glial energy metabolism, the effect that acetate supplementation has on normal brain energy stores has not been quantified. To determine the effect(s) that an increase in acetyl-CoA levels has on brain energy metabolism, we measured brain nucleotide, phosphagen and glycogen levels, and quantified cardiolipin content and mitochondrial number in rats subjected to acetate supplementation. Acetate supplementation was induced with glyceryl triacetate (GTA) by oral gavage (6 g/kg body weight). Rats used for biochemical analysis were euthanized using head-focused microwave irradiation at 2, and 4 h following treatment to immediately stop metabolism. We found that acetate did not alter brain ATP, ADP, NAD, GTP levels, or the energy charge ratio [ECR, (ATP + 1/2 ADP)/(ATP + ADP + AMP)] when compared to controls. However, after 4 h of treatment brain phosphocreatine levels were significantly elevated with a concomitant reduction in AMP levels with no change in glycogen levels. In parallel studies where rats were treated with GTA for 28 days, we found that acetate did not alter brain glycogen and mitochondrial biogenesis as determined by measuring brain cardiolipin content, the fatty acid composition of cardiolipin and using quantitative ultra-structural analysis to determine mitochondrial density/unit area of cytoplasm in hippocampal CA3 neurons. Collectively, these data suggest that an increase in brain acetyl-CoA levels by acetate supplementation does increase brain energy stores however it has no effect on brain glycogen and neuronal mitochondrial biogenesis. ? 2013 Elsevier Ltd. All rights reserved.
机译：大鼠补充醋酸盐会增加血浆醋酸盐和脑部乙酰辅酶A的水平。尽管乙酸盐被用作研究神经胶质能量代谢的标志物，但乙酸盐补充对正常脑能量存储的影响尚未被量化。为了确定乙酰辅酶A水平增加对脑能量代谢的影响，我们测量了补充乙酸盐的大鼠的脑核苷酸，磷和糖原水平，并量化了心磷脂含量和线粒体数量。通过口服管饲法（6 g / kg体重）用三乙酸甘油酯（GTA）诱导醋酸盐补充。在治疗后第2和第4小时，使用头部聚焦微波辐射对用于生化分析的大鼠实施安乐死，以立即停止新陈代谢。我们发现，与对照组相比，乙酸盐不会改变大脑的ATP，ADP，NAD，GTP水平或能量比[ECR，（ATP + 1/2 ADP）/（ATP + ADP + AMP）]。但是，治疗4小时后，脑中磷酸肌酸水平显着升高，同时AMP水平降低，糖原水平没有变化。在通过GTA治疗大鼠28天的平行研究中，我们发现乙酸盐不会改变脑糖原和线粒体的生物发生，这是通过测量脑心磷脂含量，心磷脂的脂肪酸组成并使用定量超微结构分析确定线粒体密度来确定的/海马CA3神经元细胞质的单位面积。总的来说，这些数据表明，通过补充醋酸盐会增加脑部乙酰辅酶A水平，但确实会增加脑部能量存储，但对脑部糖原和神经元线粒体的生物发生没有影响。 ？ 2013 Elsevier Ltd.保留所有权利。

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