高血糖“代谢记忆”与糖尿病视网膜病变的关系  

Relationship between hyperglycemic ＂metabolic memory＂ and diabetic retinopathy

作　　者：万松[1] 郑卫东[1] 徐国兴[1] 黄焱[2] 

机构地区：[1]福建医科大学附属第一医院眼科,350005 [2]福建省眼科研究所

出　　处：《国际眼科纵览》2012年第6期375-378,共4页International Review of Ophthalmology

基　　金：基金项目：福建省卫生厅创新基金（2009-CX-7）;福建省自然科学基金（2011J01190）

摘　　要：大规模临床试验表明糖尿病后期血糖即使有效控制，糖尿病各种并发症仍然持续进展，即高糖“记忆”效应。高糖“记忆”引起糖尿病视网膜病变（diabeticretinopathy，DR）的机制尚不清楚，氧化应激被认为具有关键作用。高糖导致视网膜上细胞线粒体结构与功能障碍，活性氧不断释放并激活下游的多条致病通路，造成“代谢记忆”在视网膜上产生，DR不断进展。此外，非酶促糖基化作用、基因表观遗传修饰以及炎症与凋亡因素等机制也可能参与其中。Metabolic memory was demonstrated in some clinical trials that diabetic complications continued even though a successful control of blood glucose at later stages. This phenomenon has recently been defined as ＂metabolic memory＂. It is still elusive how ＂hyperglycemic memory＂ influence diabetic ret- inopathy（DR）. Among the assumed mechanisms, oxidative stress is thought to have a key role. Hyperglyce- mia induces dysfunction and destruction of mitochondria in retinal cells, so reactive oxygen species are con- stantly released and activate downstream pathways, which lead to the ＂metabolic memory＂ effect on the reti- na and the progression of DR. Furthermore, other mechanisms such as advanced glycation end products, epi- genetic changes, as well as inflammation and apoptosis factors may also be implicated in this process.

关 键 词：糖尿病视网膜病变 代谢记忆 氧化应激 高级糖基化终末产物 

分 类 号：R587.2[医药卫生—内分泌]