BEHAVIORAL PHYSIOLOGY OF BODY WEIGHT REGULATION

体重调节的行为生理学

基本信息

  • 批准号:
    3241476
  • 负责人:
  • 金额:
    $ 15.69万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1988
  • 资助国家:
    美国
  • 起止时间:
    1988-09-01 至 1993-03-31
  • 项目状态:
    已结题

项目摘要

Studies have suggested that insulin may be a regulator of food intake and body weight by acting at the central nervous system (CNS). This renewal proposal addresses the hypothesis that the ability of insulin to act as a satiety signal may change during normal growth and development, and may be abnorrnal in obesity. Studies are proposed to examine whether insulin uptake into the CNS, or insulin action-in the CNS, is altered in rats as a function of age, gender, and genetic or diet-induced obesity. Insulin uptake by brain will be assessed in vivo by measurement of steady state levels of plasma and CSF insulin during vehicle or insulin infusions. Brain capillary insulin binding sites will be measured as an in vitro estimate of specific receptor-mediated transport capacity. Regulation of these receptors has been observed by this laboratory and others and may represent a potential mechanism for regulation of insulin uptake into the CNS. Insulin action will be assessed behaviorally by measuring body weight and food intake in response to intraventricular insulin infusions. Insulin action in vitro will be assessed by measurement of insulin effects on norepinephrine uptake and post-synaptic events in the hippocampus, a brain region in which I have demonstrated insulin stimulation of phospholipid metabolism which may be mediated locally by catecholamines, as well as in the hypothalamus and olfactory bulb, two brain regions which play a major role in the regulation of food intake and body weight, and compared with changes of peripheral insulin action. Together, these studies should determine whether the effectiveness of the candidate CNS adiposity signal, insulin, is regulated by changes in its uptake and/or action in the CNS.
研究表明胰岛素可能是食物摄入的调节器

项目成果

期刊论文数量(0)
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科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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DIANNE FIGLEWICZ LATTEMANN其他文献

DIANNE FIGLEWICZ LATTEMANN的其他文献

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{{ truncateString('DIANNE FIGLEWICZ LATTEMANN', 18)}}的其他基金

Dietary fatty acids, cell signals, and sucrose intake
膳食脂肪酸、细胞信号和蔗糖摄入量
  • 批准号:
    10046298
  • 财政年份:
    2018
  • 资助金额:
    $ 15.69万
  • 项目类别:
CNS Mechanisms of Acute Hypoglycemia-Associate Autonomic Failure
急性低血糖相关自主神经衰竭的中枢神经系统机制
  • 批准号:
    8258198
  • 财政年份:
    2009
  • 资助金额:
    $ 15.69万
  • 项目类别:
CNS Mechanisms of Acute Hypoglycemia-Associate Autonomic Failure
急性低血糖相关自主神经衰竭的中枢神经系统机制
  • 批准号:
    7782818
  • 财政年份:
    2009
  • 资助金额:
    $ 15.69万
  • 项目类别:
CNS Mechanisms of Acute Hypoglycemia-Associate Autonomic Failure
急性低血糖相关自主神经衰竭的中枢神经系统机制
  • 批准号:
    7686674
  • 财政年份:
    2009
  • 资助金额:
    $ 15.69万
  • 项目类别:
BEHAVIORAL PHYSIOLOGY OF BODY WEIGHT REGULATION
体重调节的行为生理学
  • 批准号:
    7878213
  • 财政年份:
    2009
  • 资助金额:
    $ 15.69万
  • 项目类别:
CNS Mechanisms of Acute Hypoglycemia-Associate Autonomic Failure
急性低血糖相关自主神经衰竭的中枢神经系统机制
  • 批准号:
    8195898
  • 财政年份:
    2009
  • 资助金额:
    $ 15.69万
  • 项目类别:
ANTIDEPRESSANT THERAPY AND HYPOGLYCEMIA
抗抑郁治疗和低血糖
  • 批准号:
    6954866
  • 财政年份:
    2005
  • 资助金额:
    $ 15.69万
  • 项目类别:
ANTIDEPRESSANT THERAPY AND HYPOGLYCEMIA
抗抑郁治疗和低血糖
  • 批准号:
    7140214
  • 财政年份:
    2005
  • 资助金额:
    $ 15.69万
  • 项目类别:
CNS Stress Pathways and the Development of Acute HAAF
CNS 应激通路与急性 HAAF 的发展
  • 批准号:
    6645366
  • 财政年份:
    2002
  • 资助金额:
    $ 15.69万
  • 项目类别:
CNS Stress Pathways and the Development of Acute HAAF
CNS 应激通路与急性 HAAF 的发展
  • 批准号:
    6548808
  • 财政年份:
    2002
  • 资助金额:
    $ 15.69万
  • 项目类别:

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