METABOLIC CONTROL OF FEEDING BEHAVIOR
进食行为的代谢控制
基本信息
- 批准号:2838173
- 负责人:
- 金额:$ 26.63万
- 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
它们影响大鼠进食的开始。法庭先前出示的证据
研究人员建议,当食物摄入开始后,
在施用代谢抑制剂2,5-AM的情况下,存在几种
在肝细胞中可能有因果关系。更
具体来说,几种类型的实验结果已经趋于一致
强烈暗示肝脏是2,5-AM的靶点,
其他实验表明,一个关键因素(或
至少密切相关)是ATP的量减少,
肝细胞拟议的实验将把分析带到一个更
通过评估结合或游离细胞ATP是否
更多的是与饮食相关,然后确定是否减少
当通过其他方式诱导时,关键ATP池会引起就座;将确定
其他被认为通过肝脏引起进食的药物(例如,甲基
palmoxirate)与类似的肝细胞变化相关;将评估
吃东西的信号与大脑功能有关的假说
肝细胞钠泵;并将确定肝细胞
钙池是一种产生信号的手段,
肝细胞到其他细胞和CNS上。
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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{{ truncateString('MARK FRIEDMAN', 18)}}的其他基金
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