Keystone Symposia on Cellular and Molecular Basis of Metabolic Disorders Series

摘要 该提案请求支持为期5年的代谢紊乱细胞和分子基础Keystone研讨会系列会议。2010年及以后的会议将发扬Keystone研讨会在这一领域的最佳传统，包括尖端研究、动态批判性讨论、跨学科发现和解决问题、建立网络和合作，以及培养下一代调查人员。第一年有六次会议。脂肪组织生物学会议讨论了血管生成在脂肪组织扩张中的作用；白色脂肪-棕色脂肪的争论；生物钟对协调食物摄入和代谢平衡活动的激素和神经信号的贡献；以及中枢和外周信号在抗精神病药物和抗逆转录病毒药物等治疗方案引起的意外脂肪营养不良疾病中的作用。食欲、新陈代谢和体重会议的并行神经元控制解决了深入了解导致肥胖和相关疾病的体重动态平衡和功能障碍的复杂机制的迫切需要。这些联合会议利用中枢神经系统和脂肪组织之间的关键相互作用来控制能量稳态，并探索与肥胖和糖尿病发病相关的这种沟通障碍。核子 受体：信号、基因调节和癌症旨在了解核受体(NRs)的配体依赖的分子作用--包括亚细胞定位、跨基因组结合和与蛋白质组的相互作用--如何与它们在生理和病理生理过程中的作用联系起来，包括激素调节的癌症。本次会议还审查了NRs作为药物开发目标的问题。同时召开的核受体：发育、生理学和疾病会议集中讨论了核受体在发育、生理和新陈代谢中的作用，以及它们与人类疾病的关系。这强调了 整合转录调控的分子机制、正常发育和生理、疾病的发生和发展、治疗干预的方法以及由NR功能障碍引起的疾病。胰岛生物学重点讨论了胰岛研究的几个领域的进展，包括发育、再生、干细胞、转录因子、新的信号通路、细胞生物学、遗传学、基因调控、药物靶向和新兴技术。本次会议明确提出了设计有效的方法来改善2型糖尿病患者的胰腺干细胞功能和存活率，以及为1型糖尿病患者的移植产生干细胞的最终目标。同时召开的糖尿病会议通过许多不同领域的研究探索了2型糖尿病的发病机制和可能的治疗方法，并利用了遗传学、基因组和生理学的观点。其目的是解决2型糖尿病及其相关代谢紊乱发生的复杂生物学基础。会议还讨论了旨在深入研究2型糖尿病分子发病机制的新技术进展。

ABSTRACT This proposal requests support for a 5-year Keystone Symposia meeting series on the Cellular and Molecular Basis of Metabolic Disorders. The meetings for 2010 and beyond will build upon the best of Keystone Symposia's tradition in this area including cutting-edge research, dynamic critical discussions, interdisciplinary discovery and problem-solving, building networks and collaborations, and developing the next generation of investigators. Year 1 consists of six meetings. The Adipose Tissue Biology meeting considers the role of angiogenesis in adipose tissue expansion; the white fat-brown fat debate; the contribution of the circadian clock to hormonal and neural signals coordinating food intake and activity for metabolic balance; and the role of central and peripheral signals in the unanticipated lipodystrophic disorders resulting from such therapeutic regimens as antipsychotics and anti-retrovirals. The concurrent Neuronal Control of Appetite, Metabolism and Weight meeting addresses the crucial need for deeper understanding of the complex mechanisms of body weight homeostasis and dysfunctions leading to obesity and associated disorders. These joint meetings take advantage of critical interaction between the CNS and adipose tissue for control of energy homeostasis, and exploring dysfunction in this communication associated with the onset of obesity and diabetes. Nuclear Receptors: Signaling, Gene Regulation, and Cancer aims to understand how the ligand-dependent molecular actions of Nuclear Receptors (NRs) - including subcellular localization, binding across the genome, and interaction with the proteome - connect to their roles in physiological and pathophysiological processes, including hormone-regulated cancers. This meeting also examines NRs as targets for drug development. The concurrent Nuclear Receptors: Development, Physiology and Disease meeting focuses on the roles of NRs in development, physiology, and metabolism, and on their involvement in human disease. This emphasizes integration of molecular mechanisms of transcriptional control, normal development and physiology, disease initiation and progression, approaches to therapeutic intervention, and diseases that arise from NR dysfunction. Islet Biology critically discusses advances in several areas of islet research including development, regeneration, stem cells, transcription factors, novel signaling pathways, cell biology, genetics, gene regulation, drug targeting, and emerging technologies. This meeting explicitly addresses the ultimate goal of designing effective approaches to improve pancreatic ss-cell function and survival in Type 2 diabetes and generating ss-cells for transplantation in Type 1 diabetes. The concurrent Diabetes meeting explores Type 2 diabetes pathogenesis and possible therapeutics via research in many different fields, and capitalizes on genetic, genomic and physiological perspectives. The aim is to resolve the complex biology underpinning development of Type 2 diabetes and its associated metabolic disorders. The meeting also discusses new technical advances designed to penetrate the molecular pathogenesis of Type 2 diabetes.