"Hyperglycemic Memory": Observational Evidence to Experimental Inference.

IF 2.4 Q3 ENDOCRINOLOGY & METABOLISM
Mohsen Ahmadi, Soudeh Ghafouri-Fard, Parisa Najari-Hanjani, Firouzeh Morshedzadeh, Tahereh Malakoutian, Mohsen Abbasi, Hounaz Akbari, Mahsa Mohammad Amoli, Negin Saffarzadeh
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引用次数: 0

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.

"高血糖记忆":从观察证据到实验推论。
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,血糖曲线并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 "概念被认为是糖尿病晚期并发症病理生物学的额外影响因素。在重要的糖尿病随机对照临床试验(包括 DCCT/EDIC 和 UKPDS)的扩展阶段,研究得出的结论是,糖尿病发病初期的血糖或代谢控制质量可在随后的糖尿病病程中保持其保护性或有害影响。目前还没有可靠的证据表明,瞬时暴露于特定的葡萄糖浓度水平会在分子水平上诱发目标组织产生一致的细胞反应。一些生物现象,如高级糖化终产物(AGEs)的产生和浓度、活性氧(ROS)和蛋白激酶 C(PKC)通路的激活、表观遗传学变化,以及最后由 miRNAs 介导的通路,可能是形成高血糖记忆的原因。本研究总结了以往实验的证据,这些证据可以从分子角度证明高血糖记忆的合理性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Current diabetes reviews
Current diabetes reviews ENDOCRINOLOGY & METABOLISM-
CiteScore
6.30
自引率
0.00%
发文量
158
期刊介绍: Current Diabetes Reviews publishes frontier reviews on all the latest advances on diabetes and its related areas e.g. pharmacology, pathogenesis, complications, epidemiology, clinical care, and therapy. The journal"s aim is to publish the highest quality review articles dedicated to clinical research in the field. The journal is essential reading for all researchers and clinicians who are involved in the field of diabetes.
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