5-HT3 receptor mediation of 5-HT & CCK-induced satiation

5-HT3受体介导5-HT

• 批准号: 6932705
• 负责人: MATTHEW R HAYES
• 金额: $ 3.37万
• 依托单位: PENNSYLVANIA STATE UNIVERSITY, THE
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-06-01 至 2006-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6932705
• 关键词: body weight; cholecystokinin; eating; gene expression; hormone regulation /control mechanism; immunocytochemistry; laboratory rat; neurotransmitter transport; nutrient intake activity; obesity; predoctoral investigator; radioimmunoassay; receptor expression; satiations; serotonin; serotonin receptor; sucrose

DESCRIPTION (provided by applicant): The prevalence of obesity is growing at an unprecedented rate in countries around the world, leading to increased morbidity and economic cost. Obesity is a consequence of a long-term positive imbalance in energy intake and expenditure leading to excessive deposits of adipose tissue. Food intake is controlled by a number of within-meal satiation signals. Cholecystokinin and serotonin are two such anorectic signals that have been shown to both independently mediate meal size, as well as interact in overall satiation. The mechanisms by which 5-HT and CCK combine to enhance suppression of food intake are not completely known but recent evidence suggests that these two anorectic signals interact at 5-HT3 and CCK-A receptors; which have been shown to be involved in energy balance. In addition, 5-HT3 receptors have been shown to mediate CCK-induced satiation possibly through mechanisms involving gastric feedback; however this has yet to be investigated. The goals of this proposal are to identify the gastric involvement in 5-HT3 receptor mediation of CCK-induced satiation, as well as examine the effects on daily food intake and body weight in response to chronic elevation of circulating 5-HT and CCK.

描述（由申请人提供）：肥胖症的患病率在世界各国以前所未有的速度增长，导致发病率和经济成本增加。肥胖是能量摄入和消耗长期正失衡导致脂肪组织过度沉积的结果。食物的摄入是由一系列餐内饱足信号控制的。胆囊收缩素和5-羟色胺是两种这样的厌食信号，它们已被证明既独立地介导进食量，又在总体饱足感中相互作用。5-HT和CCK联合收割机增强食物摄入抑制的机制尚不完全清楚，但最近的证据表明，这两种厌食信号在5-HT 3和CCK-A受体上相互作用;这两种受体已被证明参与能量平衡。此外，5-HT 3受体已被证明可能通过涉及胃反馈的机制介导CCK诱导的饱食;然而，这还有待研究。本研究的目的是确定胃参与5-HT 3受体介导的CCK诱导饱食，以及检查每日食物摄入量和体重对循环5-HT和CCK慢性升高的影响。

项目成果

Serotonin type-3 receptors mediate cholecystokinin-induced satiation through gastric distension.

3 型血清素受体通过胃扩张介导胆囊收缩素诱导的饱足感。

• DOI: 10.1152/ajpregu.00002.2006
• 发表时间: 2006
• 期刊: American journal of physiology. Regulatory, integrative and comparative physiology
• 作者: Hayes,MatthewR;Chory,FionaM;Gallagher,ClaireA;Covasa,Mihai
• 通讯作者: Covasa,Mihai