Rhodes Christopher J
Pacific Northwest Research Institute, 720 Broadway, Seattle, WA 98122, USA.
Science. 2005 Jan 21;307(5708):380-4. doi: 10.1126/science.1104345.
In type 2 diabetes, the beta cells of the pancreas fail to produce enough insulin to meet the body's demand, in part because of an acquired decrease in beta-cell mass. In adults, pancreatic beta-cell mass is controlled by several mechanisms, including beta-cell replication, neogenesis, hypertrophy, and survival. Here, I discuss evidence supporting the notion that increased beta-cell apoptosis is an important factor contributing to beta-cell loss and the onset of type 2 diabetes. Interestingly, a key signaling molecule that promotes beta-cell growth and survival, insulin receptor substrate 2 (IRS-2), is a member of a family of proteins whose inhibition contributes to the development of insulin resistance in the liver and other insulin-responsive tissues. Thus, the IRS-2 pathway appears to be a crucial participant in the tenuous balance between effective pancreatic beta-cell mass and insulin resistance.
在2型糖尿病中,胰腺的β细胞无法产生足够的胰岛素来满足身体需求,部分原因是β细胞数量的后天减少。在成年人中,胰腺β细胞数量受多种机制控制,包括β细胞复制、新生、肥大和存活。在此,我讨论支持以下观点的证据:β细胞凋亡增加是导致β细胞丢失和2型糖尿病发病的重要因素。有趣的是,一种促进β细胞生长和存活的关键信号分子——胰岛素受体底物2(IRS-2),是一类蛋白质家族的成员,对其抑制会导致肝脏和其他胰岛素反应性组织中胰岛素抵抗的发展。因此,IRS-2途径似乎是有效胰腺β细胞数量与胰岛素抵抗之间脆弱平衡的关键参与者。