Abstract：
Several epidemiological studies have appreciated the impact of \"duration\" and \"level\" of hyperglycemia on the initiation and development of chronic complications of diabetes. However, glycemic profiles could not fully explain the presence/absence and severity of diabetic complications. Genetic issues and concepts of \"hyperglycemic memory\" have been introduced as additional influential factors involved in the pathobiology of late complications of diabetes. In the extended phase of significant diabetes randomized, controlled clinical trials, including DCCT/EDIC and UKPDS, studies have concluded that the quality of glycemic or metabolic control at the early time around the diabetes onset could maintain its protective or detrimental impact throughout the following diabetes course. There is no reliable indication of the mechanism by which the transient exposure to a given glucose concentration level could evoke a consistent cellular response at target tissues at the molecular levels. Some biological phenomena, such as the production and the concentration of advanced glycation end products (AGEs), reactive oxygen species (ROS) and protein kinase C (PKC) pathway activations, epigenetic changes, and finally, the miRNAs-mediated pathways, may be accountable for the development of hyperglycemic memory. This work summarizes evidence from previous experiments that may substantiate the hyperglycemic memory soundness by its justification in molecular terms.
摘要：
一些流行病学研究已经认识到高血糖的“持续时间”和“水平”对糖尿病慢性并发症的发生和发展的影响。然而,血糖分析不能完全解释糖尿病并发症的存在/不存在和严重程度.遗传问题和“高血糖记忆”的概念已被引入，作为涉及糖尿病晚期并发症病理生物学的其他影响因素。在显著的糖尿病随机化的延长阶段，对照临床试验,包括DCCT/EDIC和UKPDS，研究已经得出结论,糖尿病发病早期的血糖或代谢控制质量可以在整个糖尿病病程中保持其保护性或有害影响.对于在分子水平上瞬时暴露于给定葡萄糖浓度水平可以在靶组织引起一致的细胞反应的机制,没有可靠的指示。一些生物学现象,例如糖基化终产物(AGEs)的产生和浓度，活性氧（ROS）和蛋白激酶C（PKC）途径激活，表观遗传变化,最后，miRNA介导的途径，可能对高血糖记忆的发展负责。这项工作总结了先前实验的证据，这些证据可能通过分子方面的理由来证实高血糖记忆的正确性。
