Profil Institut für Stoffwechselforschung, Hellersbergstrasse 9, 41460 Neuss, Germany.
Cardiovasc Diabetol. 2010 Sep 14;9:51. doi: 10.1186/1475-2840-9-51.
Multiple and complex pathways promote the deleterious effects of hyperglycemia in diabetes, ultimately leading to micro- and macrovascular disease. Some of the known mechanisms in diabetic vascular disease may explain the initiation of the "metabolic memory", but fall short if long periods of time are involved.Vascular research has been prolific in the past in finding links between microvascular dysfunction and subsequent macrovascular disease. Thus, this text will extend the current discussion of the "metabolic memory" by including available data from vascular research.The hypothesis proposes that structural and functional changes in the microcirculation interact within the vascular continuum with larger arteries. This interaction may lead to subsequent upstream endothelial dysfunction, atherosclerosis and vascular complications ("Micro/Macro Interaction"). The underlying microvascular structural changes may be more long-term and possibly mediate the "metabolic memory".This hypothesis, that the "not-so new" interaction between micro-and macrovasculature may promote "metabolic memory" effects extends and unifies currently discussed theories.
多种复杂的途径促进了高血糖在糖尿病中的有害作用，最终导致微血管和大血管疾病。糖尿病血管疾病的一些已知机制可以解释“代谢记忆”的启动，但如果涉及很长一段时间，则还不够充分。过去，血管研究在发现微血管功能障碍与随后的大血管疾病之间的联系方面硕果累累。因此，本文将通过纳入血管研究中的现有数据，扩展对“代谢记忆”的当前讨论。该假说提出，微循环中的结构和功能变化在血管连续体中与较大的动脉相互作用。这种相互作用可能导致随后的上游内皮功能障碍、动脉粥样硬化和血管并发症（“微/大相互作用”）。潜在的微血管结构变化可能更长期，并且可能介导“代谢记忆”。该假说认为，微血管和大血管之间“并非全新”的相互作用可能促进“代谢记忆”效应，它扩展和统一了目前讨论的理论。
