NUTRITION, LIPOPROTEIN LIPASE AND BODY WEIGHT REGULATION
营养、脂蛋白脂肪酶和体重调节
基本信息
- 批准号:2870321
- 负责人:
- 金额:$ 21.07万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1990
- 资助国家:美国
- 起止时间:1990-01-01 至 1998-11-30
- 项目状态:已结题
- 来源:
- 关键词:Schwann cells appetite regulatory center bioenergetics body weight brain circulation brain electrical activity central nervous system chylomicrons glia immunoprecipitation laboratory rat lipid metabolism lipoprotein lipase mixed tissue /cell culture myelination neural transmission nutrition related tag synapses
项目摘要
DESCRIPTION (Adapted from Applicant's Abstract): The studies will
determine: (1) the cells of synthesis of lipoprotein lipase (LPL) within
the spinal cord and peripheral nerve, and the function of LPL in these
sites. It is postulated that LPL is made by oligodendrocytes in the
spinal cord and by Schwann cells in peripheral nerve, and that LPL in
the nervous system predominantly works to facilitate the provision of
fatty acids for membrane phospholipid synthesis; (2) mechanisms for the
localization of LPL protein in the brain. It is postulated that the
distribution of LPL protein on the capillary endothelium throughout the
brain is a consequence of delivery of the lipase by the circulation; and
(3) the function of LPL in regions of the brain wherein LPL is
synthesized. Because LPL mRNA has been localized to a number of cell
types in the brain including neurons in the hippocampus, Purkinje cells
of the cerebellum and cells deep within the cortex, it is postulated
that lipolysis products, i.e. fatty acids, derived by the action of LPL
on triglyceride-rich lipoproteins within these sites, will enhance
membrane excitability. Although glucose is the predominant fuel for the
central nervous system (CNS), recent reports indicate that changes in
fatty acid oxidation within the hypothalamus reflect changes in energy
balance. Moreover, inhibition of fatty acid oxidation inhibits feeding.
Because plasma triglyceride-rich lipoproteins increase with feeding, an
LPL-dependent pathway could function in certain brain regions as a
signal for satiety. Moreover, synaptic transmission by triglyceride-
rich lipoprotein triglyceride fatty acids could generate metabolic
memory which relates to body weight regulation. Overall, these studies
should provide a comprehensive approach to explain the presence of LPL
in the nervous system.
描述(改编自申请人摘要):研究将
确定:(1)合成脂蛋白脂酶(LPL)的细胞内
以及LPL在脊髓和周围神经中的作用
网站. 据推测,LPL是由大脑中的少突胶质细胞产生的。
脊髓和周围神经中雪旺细胞,以及LPL
神经系统的主要功能是提供
膜磷脂合成的脂肪酸;(2)膜磷脂合成的机制
LPL蛋白在脑中的定位。 据推测,
LPL蛋白在毛细血管内皮上的分布
脑是脂肪酶通过循环输送的结果;
(3)LPL在LPL被激活的脑区域中的功能
合成了 由于LPL mRNA定位于许多细胞,
包括海马神经元、浦肯野细胞
小脑和皮层深处的细胞,
通过LPL的作用衍生的脂解产物,即脂肪酸,
在这些位点内的富含磷脂酰肌醇的脂蛋白上,
膜兴奋性 虽然葡萄糖是主要的燃料,
中枢神经系统(CNS),最近的报告表明,
下丘脑内的脂肪酸氧化反应了能量的变化
平衡此外,脂肪酸氧化的抑制抑制摄食。
因为血浆富含磷脂酰肌醇的脂蛋白随着进食而增加,
LPL依赖性通路可能在某些脑区起作用,
表示饱足。 此外,通过甘油三酯-
丰富的脂蛋白甘油三酯脂肪酸可以产生代谢
涉及体重调节的记忆。 总的来说,这些研究
应该提供一个全面的方法来解释LPL的存在
在神经系统中。
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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Robert H Eckel其他文献
Cardio-renal-metabolic disease in primary care setting.
初级保健机构中的心肾代谢疾病。
- DOI:
- 发表时间:
2023 - 期刊:
- 影响因子:0
- 作者:
Mahmoud Ibrahim;Ebtesam M Ba;Jason Baker;A. Cahn;Antonio Ceriello;Francesco Cosentino;M. J. Davies;Robert H Eckel;Luc Van Gaal;Peter Gaede;Y. Handelsman;Samuel Klein;Richard David Leslie;Paolo Pozzilli;Stefano Del Prato;F. Prattichizzo;Oliver Schnell;P. Seferovic;E. Standl;Abraham Thomas;Jaakko Tuomilehto;P. Valensi;Guillermo E. Umpierrez - 通讯作者:
Guillermo E. Umpierrez
<sup>1</sup><sup>2</sup>The glycemic index at 20 y<sup>,</sup>
- DOI:
10.1093/ajcn/76/1.264s - 发表时间:
2002-07-01 - 期刊:
- 影响因子:
- 作者:
David S Ludwig;Robert H Eckel - 通讯作者:
Robert H Eckel
Regular-fat and low-fat dairy foods and cardiovascular diseases: perspectives for future dietary recommendations
全脂和低脂乳制品与心血管疾病:对未来膳食建议的展望
- DOI:
10.1016/j.ajcnut.2025.03.009 - 发表时间:
2025-05-01 - 期刊:
- 影响因子:6.900
- 作者:
Benoît Lamarche;Arne Astrup;Robert H Eckel;Emma Feeney;Ian Givens;Ronald M Krauss;Philippe Legrand;Renata Micha;Marie-Caroline Michalski;Sabita Soedamah-Muthu;Qi Sun;Frans J Kok - 通讯作者:
Frans J Kok
Definition and diagnostic criteria of clinical obesity
临床肥胖的定义和诊断标准
- DOI:
10.1016/s2213-8587(24)00316-4 - 发表时间:
2025-03-01 - 期刊:
- 影响因子:41.800
- 作者:
Francesco Rubino;David E Cummings;Robert H Eckel;Ricardo V Cohen;John P H Wilding;Wendy A Brown;Fatima Cody Stanford;Rachel L Batterham;I Sadaf Farooqi;Nathalie J Farpour-Lambert;Carel W le Roux;Naveed Sattar;Louise A Baur;Katherine M Morrison;Anoop Misra;Takashi Kadowaki;Kwang Wei Tham;Priya Sumithran;W Timothy Garvey;John P Kirwan;Geltrude Mingrone - 通讯作者:
Geltrude Mingrone
<sup>1</sup><sup>2</sup>The glycemic index at 20 y<sup>,</sup>
- DOI:
10.1093/ajcn/76.1.264s - 发表时间:
2002-07-01 - 期刊:
- 影响因子:
- 作者:
David S Ludwig;Robert H Eckel - 通讯作者:
Robert H Eckel
Robert H Eckel的其他文献
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{{ truncateString('Robert H Eckel', 18)}}的其他基金
Obesity and Cardiovascular Disease: Opportunity for Post-Doctoral Training
肥胖与心血管疾病:博士后培训的机会
- 批准号:
9293351 - 财政年份:2014
- 资助金额:
$ 21.07万 - 项目类别:
Obesity and Cardiovascular Disease: Opportunity for Post-Doctoral Training
肥胖与心血管疾病:博士后培训的机会
- 批准号:
9390657 - 财政年份:2014
- 资助金额:
$ 21.07万 - 项目类别:
Obesity and Cardiovascular Disease: Opportunity for Post-Doctoral Training
肥胖与心血管疾病:博士后培训的机会
- 批准号:
9064837 - 财政年份:2014
- 资助金额:
$ 21.07万 - 项目类别:
Obesity and Cardiovascular Disease: Opportunity for Post-Doctoral Training
肥胖与心血管疾病:博士后培训的机会
- 批准号:
8845604 - 财政年份:2014
- 资助金额:
$ 21.07万 - 项目类别:
Mechanisms of Obesity in Mice with Neuron-Specific Lipoprotein Lipase Deficiency
神经元特异性脂蛋白脂肪酶缺乏小鼠的肥胖机制
- 批准号:
8280420 - 财政年份:2011
- 资助金额:
$ 21.07万 - 项目类别:
Mechanisms of Obesity in Mice with Neuron-Specific Lipoprotein Lipase Deficiency
神经元特异性脂蛋白脂肪酶缺乏小鼠的肥胖机制
- 批准号:
8668938 - 财政年份:2011
- 资助金额:
$ 21.07万 - 项目类别:














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