In vivo Metabolism of Liver and Heart

1.利用培养的神经元，我们操纵细胞内钠浓度作为活性的标志。莫能菌素引起的细胞内钠升高刺激钠泵消耗三磷酸腺苷。紧接着，线粒体衍生的氧化磷酸化酶的转录上调，这将导致ATP合成增加。本研究确定了线粒体的电活动、ATP消耗和氧化-磷酸化激活之间的快速耦合机制，以合成新的ATP。(Mehrabian等人，2005年)。 2.以6-羟基多巴胺(6-OHDA)为交感神经去神经模型，建立帕金森病心脏交感神经失神经模型。将我们的活体模型扩展到大脑，我们测量了去神经和正常心脏的磷脂中棕榈酸和花生四烯酸的掺入。棕榈酸的掺入(来自酰基辅酶A前体池)没有变化，而花生四烯酸的掺入减少了70%，伴随着磷脂酶A2活性的降低。现在，使用正电子发射断层扫描来观察帕金森病患者是否有这种去神经缺陷将是有兴趣的。(Patrick等人，2005)

1. Using cultured neurons, we manipulated intracellular sodium concentrations as a marker of activity. Increased intracellular sodium caused by monensin stimulated the sodium pump to consume ATP. Immediately thereafter, transcription of mitochondrial-derived enzymes for oxidative phosphorylation was upregulated, which would lead to increased ATP synthesis. This study identified the rapid coupling mechanism between electrical activity, ATP consumption and oxidative-phosphorylation activation in mitochondria for new ATP synthesis. (Mehrabian et al 2005). 2. As a model for heart sympathetic denervation in Parkinson disease, rats were sympathetically denervated with 6-hydroxydopamine (6-OHDA). Extending our in vivo model for the brain, we measured incorporation of palmitic and arachidonic acids into phospholipids of denervated and normal hearts. Incorporation of palmitic acid (from the acyl-CoA precursor pool) was unchanged, whereas incorporation of arachidonic acid was reduced by 70%, accompanied by a reduction in phospholipase A2 activity. It now would be of interest to see if Parkinson disease patients have this denervation defect, using positron emission tomography. (Patrick et al 2005)