Hindbrain integration of adiposity and satiety signals

肥胖和饱腹感信号的后脑整合

• 批准号: 7077584
• 负责人: Diana L Williams
• 金额: $ 5.48万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-07-01 至 2008-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7077584
• 关键词: adipocytes; adipose tissue; behavioral /social science research tag; body composition; brain mapping; cell cell interaction; cholecystokinin; hormone regulation /control mechanism; laboratory rat; leptin; neural information processing; nutrient intake activity; nutrition related tag; postdoctoral investigator; rhombencephalon; satiations

DESCRIPTION (provided by applicant): This proposal investigates the neural circuitry that integrates input from the adiposity hormone, leptin, and the gut-derived satiety signals, cholecystokinin (CCK), in the control of food intake. Available data provides compelling support for the hypothesis that leptin reduces food intake in part by enhancing satiety and hindbrain responses to gastrointestinal signals, including CCK. Here, we propose to identify the specific subset of hindbrain neurons whose responses to CCK are stimulated by leptin. Second, we will determine whether the interaction between leptin and CCK, clearly demonstrated with pharmacological doses of leptin, occurs with physiological changes in leptin levels. Finally, we will determine whether leptin regulates hindbrain cell responsiveness to CCK through a direct action within the caudal brainstem or through an indirect route, perhaps involving a descending projection from the forebrain. Together, these studies will help to clarify how changes in body fat stores lead to compensatory adjustments of meal size and thus have the potential to significantly advance our understanding of the neural circuitry that regulates energy balance.

描述（由申请人提供）：该提案研究了从脂肪激素，瘦素和肠道衍生的饱腹感信号胆囊化（CCK）中整合输入的神经回路，以控制食物摄入量。可用的数据为瘦素的假设提供了令人信服的支持，即瘦素可以通过增强饱腹感和对胃肠道信号（包括CCK）的后代反应来降低食物摄入量。在这里，我们建议识别瘦素刺激对CCK反应的后脑神经元的特定子集。其次，我们将确定瘦素和CCK之间的相互作用是否与瘦素的药理剂量清楚地证明了瘦素水平的生理变化。最后，我们将通过尾脑干内的直接作用或通过间接途径来确定瘦素是调节对CCK的后脑细胞对CCK的反应，也许涉及前脑的下降投影。总之，这些研究将有助于阐明体内脂肪储存的变化如何导致膳食大小的补偿性调整，从而有可能显着提高我们对调节能量平衡的神经回路的理解。