Towards Understanding Islet Biology

描述(由申请人提供)： 在过去的十年里，人们对朗格汉斯胰岛的生物学兴趣迅速增长。活动激增在很大程度上是由于糖尿病发病率的迅速增加，以及胰岛内胰岛素分泌细胞(β细胞)衰竭在这两种主要疾病的发病机制中所起的关键作用。这次研讨会将特别聚焦于2型糖尿病的β细胞衰竭的机制，这种疾病正迅速成为一种世界性的流行病(仅在美国就估计有1800万人患病)。β细胞衰竭现在被认为是触发从糖尿病前期/代谢综合征向完全的2型糖尿病转变的事件。我们在了解基本的β细胞生物学、2型糖尿病中β细胞功能丧失和丢失的机制以及开发新的策略以增强糖尿病动物和人类的β细胞生存和功能方面取得了重大进展。这些进展值得以Keystone研讨会的形式进行仔细的审查和讨论，我们预计将吸引该领域最优秀的科学家参加。最近在知识方面的这些进步都是基于学术和工业贡献者的贡献，我们的会议计划包括向这两个部门的关键贡献者发出的计划邀请。会议将分为三个主要部分：A)综述对基本的β细胞生物学的了解进展，包括燃料刺激的胰岛素分泌机制和受体介导的过程在增强燃料驱动的反应中的作用；B)代谢燃料失衡引起的β细胞功能障碍和破坏的机制，包括高脂血症、高血糖和应激反应的作用；C)改善β细胞功能的靶点和新的技术途径。总而言之，我们相信，这一计划将及时和有价值地促进糖尿病研究的进展，糖尿病在世界各地的流行比例已经增加，以这样或那样的方式影响到几乎每个民族和种族群体。尽管在过去的几十年里，我们对胰岛素作用的了解有了很大的提高，但我们对导致临床糖尿病的主要决定因素--β细胞失败的原因的理解却并非如此。除非我们更好地了解是什么调节了胰岛素的释放，以及是什么让这些β细胞停止工作，否则要改进目前的诊断和治疗工具将是非常困难的。我们认为，这次会议将为胰岛生物学领域提供一个全面讨论的论坛，携手开展广泛的健康教育计划，并有望改变这种疾病对我们社会的影响。

DESCRIPTION (provided by applicant): The past decade has seen a burgeoning of interest in the biology of the pancreatic islets of Langerhans. The surge in activity is driven in large measure by the rapid increase in the incidence of diabetes, and the critical role of failure of the insulin secreting cells (beta-cells) within the pancreatic islets in the pathogenesis of both major forms of the disease. This symposium will focus specifically on mechanisms of beta-cell failure in type 2 diabetes, which is fast becoming an epidemic disease world-wide (estimated prevalence in the United States alone, 18 million people). Beta-cell failure is now recognized as the event that triggers the transition from pre-diabetes/metabolic syndrome to full-blown type 2 diabetes. Major advances have occurred in our understanding of fundamental beta-cell biology, mechanisms of loss of function and loss of beta-cell mass in type 2 diabetes, and development of new strategies for enhancing beta-cell survival and function in diabetic animals and humans. These advances deserve careful review and discussion in the form of a Keystone symposium to which we expect to attract the very best scientists in the field. These recent advances in knowledge have occurred based on contributions of academic and industrial contributors alike, and our meeting plan includes projected invitations to key contributors from both sectors. The meeting will be divided into three major sections: A) Review of recent progress in understanding of basic beta-cell biology, including mechanisms of fuel-stimulated insulin secretion and the role of receptor-mediated processes in potentiation of fuel-driven responses; B) Mechanisms of beta-cell dysfunction and destruction in response to metabolic fuel imbalance, including the roles of hyperlipidemia, hyperglycemia, and stress responses; C) Targets for improvement of beta cell function and new technological approaches. In sum, we believe that this program will be a timely and valuable contributor to advancement of a research Diabetes Mellitus has increased in epidemic proportions all over the world, affecting in one way or another almost every ethnic and racial group. Although our knowledge on Insulin Action has enormously increased in the last few decades, this is not the case with our understanding of what makes a beta cell fail, the main determinant of clinical diabetes. Until we have a better understanding on what regulates insulin release and what makes these beta cells stop working, it will be very difficult to improve current diagnostic and therapeutic tools. We think that this meeting will provide a forum for comprehensive discussions in the field of islet biology hand in hand with extensive programs in health education, and hopefully change the impact of this disease on our society.