The role of sweet taste genes in postingestive endocrine responses to sweeteners

描述（由申请人提供）：味觉是决定食物或饮料是否被摄入或拒绝的主要感官系统。味道也影响食物的消化和代谢。因此，了解这种感觉背后的机制对于我们控制营养摄入和调节导致肥胖、高血压和代谢综合征等疾病的过度消耗的能力至关重要。这些疾病对人类健康构成严重问题，并在世界范围内，包括在美国和俄罗斯，造成重大的负面经济影响。该项目的长期目标是定位克隆与味觉和摄食行为有关的基因。这包括开发用于基因定位和机制研究的遗传定义小鼠模型。这项FIRCA提案将扩展这些研究，以检查甜味基因在摄取后对甜味剂的内分泌反应中的作用。这些研究将有助于在小鼠中进行基因鉴定，从而揭示其人类同源物的功能及其在味觉相关人类行为中的作用。该项目将支持莫奈尔中心和巴甫洛夫研究所的科学家之间的合作，并将帮助建立巴甫洛夫研究所的研究能力。拟议的研究将主要在俄罗斯俄罗斯科学院的巴甫洛夫生理学研究所进行，与Zolotarev博士合作，作为NIH拨款R01DC000882的延伸（2008年9月19日至2013年8月31日）。小灵通398/2590 （Rev. 09/04，重新发布4/2006）页延续格式页

DESCRIPTION (provided by applicant): Taste is the primary sensory system that determines whether a food or beverage will be ingested or rejected. Taste also influences the digestion and metabolism of food. Consequently, understanding the mechanisms underlying this sense is central to our ability to control intake of nutrients and modulate the excesses of consumption that contribute to diseases such as obesity, hypertension and the metabolic syndrome. These diseases pose serious problems for human health and have major negative economic impact worldwide, including in the United States and Russia. The long-term goal of the parent project is to positionally clone genes involved in taste and ingestive behavior. This involves developing genetically defined mouse models for genetic mapping and mechanistic studies. This FIRCA proposal will expand these studies to examine the role of sweet taste genes in postingestive endocrine responses to sweeteners. The proposed studies will aid in gene identification in mice, which will reveal the function of their human orthologs and their role in taste-related human behavior. This project will support collaboration between scientists at the Monell Center and the Pavlov Institute and will help to build research capabilities at the Pavlov Institute. The propose research will be done primarily in Russia at the Pavlov Institute of Physiology of the Russian Academy of Sciences in collaboration with Dr. Zolotarev as an extension of NIH grant R01DC000882 (09/19/2008 - 08/31/2013). PHS 398/2590 (Rev. 09/04, Reissued 4/2006) Page Continuation Format Page