Towards Understanding Islet Biology

描述（由申请人提供）： 在过去的十年里，人们对胰岛生物学的兴趣迅速增长。活动的激增在很大程度上是由糖尿病发病率的快速增加以及胰岛内胰岛素分泌细胞（β细胞）的衰竭在两种主要形式的疾病的发病机制中的关键作用驱动的。本次研讨会将特别关注2型糖尿病中β细胞衰竭的机制，2型糖尿病正在迅速成为世界范围内的流行病（仅在美国估计患病率为1800万人）。β-细胞衰竭现在被认为是引发从糖尿病前期/代谢综合征转变为全面的2型糖尿病的事件。在我们对基本β细胞生物学、2型糖尿病中β细胞功能丧失和质量丧失的机制的理解，以及在糖尿病动物和人类中增强β细胞存活和功能的新策略的开发方面，已经取得了重大进展。这些进展值得以Keystone研讨会的形式进行仔细的审查和讨论，我们希望吸引该领域最优秀的科学家。这些最新的知识进步是基于学术和工业贡献者的贡献而发生的，我们的会议计划包括对这两个部门的关键贡献者的预计邀请。会议将分为三个主要部分：A）回顾对基本β细胞生物学的最新进展，包括燃料刺激胰岛素分泌的机制和受体介导的过程在增强燃料驱动反应中的作用; B）代谢燃料失衡引起β细胞功能障碍和破坏的机制，包括高脂血症、高血糖症和应激反应的作用; C）改善β细胞功能的目标和新的技术方法。总之，我们相信，这一计划将是一个及时和宝贵的贡献，以促进研究糖尿病已增加流行病的比例在世界各地，以这样或那样的方式影响几乎每一个民族和种族群体。虽然我们对胰岛素作用的了解在过去几十年中有了很大的增加，但我们对β细胞失败的理解并非如此，β细胞是临床糖尿病的主要决定因素。在我们更好地了解是什么调节胰岛素释放以及是什么使这些β细胞停止工作之前，很难改善目前的诊断和治疗工具。我们认为，这次会议将为胰岛生物学领域的全面讨论提供一个论坛，并与广泛的健康教育计划携手并进，希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.