Prentki Marc, Nolan Christopher J
Molecular Nutrition Unit and Montreal Diabetes Research Center, University of Montreal and Centre Hospitalier de l'Université de Montréal, Montreal, Quebec, Canada.
J Clin Invest. 2006 Jul;116(7):1802-12. doi: 10.1172/JCI29103.
The major focus of this Review is on the mechanisms of islet beta cell failure in the pathogenesis of obesity-associated type 2 diabetes (T2D). As this demise occurs within the context of beta cell compensation for insulin resistance, consideration is also given to the mechanisms involved in the compensation process, including mechanisms for expansion of beta cell mass and for enhanced beta cell performance. The importance of genetic, intrauterine, and environmental factors in the determination of "susceptible" islets and overall risk for T2D is reviewed. The likely mechanisms of beta cell failure are discussed within the two broad categories: those with initiation and those with progression roles.
本综述的主要重点是肥胖相关2型糖尿病(T2D)发病机制中胰岛β细胞功能衰竭的机制。由于这种细胞死亡发生在β细胞对胰岛素抵抗进行代偿的背景下,因此还探讨了代偿过程中涉及的机制,包括β细胞量增加的机制和β细胞功能增强的机制。本文综述了遗传、子宫内和环境因素在确定“易感”胰岛及T2D总体风险中的重要性。β细胞功能衰竭的可能机制在两大类中进行了讨论:具有起始作用的机制和具有进展作用的机制。