METABOLIC CONTROL OF FEEDING BEHAVIOR
进食行为的代谢控制
基本信息
- 批准号:2639736
- 负责人:
- 金额:$ 28.99万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1993
- 资助国家:美国
- 起止时间:1993-08-01 至 2001-11-30
- 项目状态:已结题
- 来源:
- 关键词:adenosine triphosphate antimetabolites behavior prediction bioenergetics calcium flux carbohydrate analog laboratory rat liver cells liver metabolism mannitol nuclear magnetic resonance spectroscopy nutrient intake activity nutrition related tag ouabain psychobiology sodium potassium exchanging ATPase
项目摘要
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.
这是一项额外五年支持的请求
涉及肝脏代谢亚细胞变化的实验以及如何
它们影响大鼠的进餐时间。先前提供的证据
研究人员建议,当进食后开始
施用代谢抑制剂 2, 5-AM,有几种
与肝细胞相关,很可能具有因果作用。更多的
具体来说,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
外生作用;和其他实验表明,一个关键因素(或
至少密切相关)是 ATP 量的减少
肝细胞。拟议的实验将使分析更加深入
通过评估结合或游离细胞 ATP 是否还原水平
与饮食更相关,然后确定是否减少
关键 ATP 池在通过其他方式诱导时会引发座位;将确定是否
其他被认为通过肝脏进食的药物(例如甲基
palmoxirate)与类似的肝细胞变化相关;将评估
假设进食信号与大脑功能有关
肝细胞钠泵;并确定肝细胞是否发生变化
钙池是一种产生信号的方法,该信号可以从
肝细胞到其他细胞和中枢神经系统。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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MARK FRIEDMAN其他文献
MARK FRIEDMAN的其他文献
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