Martens Geert A, Pipeleers Daniel
Brussels Free University, Brussels, Belgium.
Vitam Horm. 2009;80:507-39. doi: 10.1016/S0083-6729(08)00617-1.
The key role of glucose in regulating insulin release by the pancreatic beta cell population is not only dependent on acute stimulus-secretion coupling mechanisms but also on more long-term influences on beta cell survival and phenotype. Glucose serves as a major survival factor for beta cells via at least three actions: it prevents an oxidative redox state, it suppresses a mitochondrial apoptotic program that is triggered at reduced mitochondrial metabolic activity and it induces genes needed for the cellular responsiveness to glucose and to growth factors. Glucose-regulated pathways may link protein synthetic and proliferative activities, making glucose a permissive factor for beta cell proliferation, in check with metabolic needs. Conditions of inadequate glucose metabolism in beta cells are not only leading to deregulation of acute secretory responses but should also be considered as causes for increased apoptosis and reduced formation of beta cells, and loss of their normal differentiated state.
葡萄糖在调节胰腺β细胞群释放胰岛素方面的关键作用不仅取决于急性刺激-分泌偶联机制，还取决于对β细胞存活和表型的更长期影响。葡萄糖通过至少三种作用作为β细胞的主要存活因子：它防止氧化还原状态，抑制在降低的线粒体代谢活性时触发的线粒体凋亡程序，并诱导细胞对葡萄糖和生长因子反应所需的基因。葡萄糖调节的途径可能将蛋白质合成和增殖活动联系起来，使葡萄糖成为β细胞增殖的允许因子，以符合代谢需求。β细胞中葡萄糖代谢不足的情况不仅会导致急性分泌反应失调，还应被视为细胞凋亡增加、β细胞形成减少以及其正常分化状态丧失的原因。
