METABOLIC CONTROL OF FEEDING BEHAVIOR

这是一项额外五年的支持请求，以执行 涉及肝脏代谢亚细胞变化的实验及其如何 它们会影响老鼠进餐的开始时间。提交的先前证据 研究人员建议，当食物摄取开始于 给药代谢抑制剂2，5-AM，有几种 在肝细胞中存在相关性，这很可能具有因果关系。更多 具体地说，几种类型的实验的结果已经收敛 强烈暗示肝脏是2，5-AM或 外在作用；而其他实验表明，一个关键因素(或 至少密切相关)是指在 肝细胞。拟议的实验将把分析带到更多 通过评估结合的或游离的细胞ATP是 更多地与进食有关，然后确定是否减少了 当通过其他方式诱导时，关键的ATP池将获得座位；将决定是否 其他被认为通过肝脏进食的药物(如甲基 Palmoxirate)与类似的肝细胞改变有关；将评估 关于进食的信号与大脑功能有关的假说 肝细胞的钠泵；并将决定肝细胞的变化 钙池是一种产生信号的手段，这种信号可以从 肝细胞转移到其他细胞和中枢神经系统。

This is a request for five additional years support to carry out experiments involving metabolic subcellular changes in the liver and how they influence the onset of meals in rats. Prior evidence produced by the investigator suggests that when food intake is initiated after the administration of the metabolic inhibitor, 2, 5-AM, there are several correlates in hepatocytes that may well have a causal role. More specifically, the results of several types of experiments have converged to strongly implicate that the liver is the target for 2, 5-AMs or exigenicaction; and other experiments have indicated that a key factor (or at least close correlate) is a reduction in the amount of ATP in hepatocytes. Proposed experiments will take the analysis to a more reductionistic level by assessing whether bound or free cellular ATP is more correlated with eating and by then determining if a reduction in the key ATP pool elicit seating when induced by other means; will determine if other drugs thought to elicit eating via the liver (e.g., methyl palmoxirate) are associated with similar hepatocyte changes; will assess the hypothesis that the signal to eat is associated with functioning of the hepatocyte sodium pump; and will determine if changes in hepatocyte calcium pools are a means for generating a signal that could pass from hepatocytes to other cells and on the CNS.