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慢性和急性高血糖在糖尿病并发症发展中的作用。

Role of chronic and acute hyperglycemia in the development of diabetes complications.

机构信息

Department of Paediatrics, University of Chieti, Chieti, Italy.

出版信息

Diabetes Technol Ther. 2011 Mar;13(3):389-94. doi: 10.1089/dia.2010.0146. Epub 2011 Feb 7.

DOI:10.1089/dia.2010.0146
PMID:21299400
Abstract

Chronic hyperglycemia, as assessed by hemoglobin A1c (HbA1c) levels, has been associated with the development of microvascular and macrovascular complications of diabetes. Several studies have shown that acute hyperglycemia can add to the effect of chronic hyperglycemia in inducing tissue damage. Acute hyperglycemia can activate the same metabolic and hemodynamic pathways as chronic hyperglycemia. In particular, it is associated with increased mitochondrial production of reactive oxidant species, which have been suggested as the link between hyperglycemia and the activation of downstream pathways, mediating tissue damage. Studies performed in subjects with diabetes have shown that there is a positive association between HbA1c and both fasting and postprandial glucose levels. However, it appears that the contribution of these two parameters to the total HbA1c concentrations varies according to the degree of metabolic control. Postprandial glucose excursions are predominant in patients with a good or mild glycemic control, whereas the contribution of fasting hyperglycemia is stronger as glycemic control worsens. Glucose variability, like the intra-day glucose fluctuations from peaks to nadirs, is another important parameter, which, mainly in subjects with type 2 diabetes, has emerged as an HbA1c-independent risk factor for the development of vascular complications. Based on the current knowledge on the association not only of HbA1c, but also of fasting and postprandial glucose, with diabetes complications, it is paramount that antidiabetes strategies are directed at improving all these components in order to reduce the burden associated with diabetes.

摘要

慢性高血糖(通过糖化血红蛋白 [HbA1c] 水平评估)与糖尿病的微血管和大血管并发症的发展有关。多项研究表明,急性高血糖可加重慢性高血糖引起的组织损伤。急性高血糖可激活与慢性高血糖相同的代谢和血流动力学途径。特别是,它与线粒体产生的活性氧化物质增加有关,这些物质被认为是高血糖与下游途径激活之间的联系,介导组织损伤。在糖尿病患者中进行的研究表明,HbA1c 与空腹和餐后血糖水平之间存在正相关。然而,这两个参数对总 HbA1c 浓度的贡献似乎根据代谢控制的程度而有所不同。在血糖控制良好或轻度的患者中,餐后血糖波动占主导地位,而随着血糖控制恶化,空腹高血糖的贡献更强。葡萄糖变异性(如从峰值到谷值的日内血糖波动)是另一个重要参数,特别是在 2 型糖尿病患者中,它已成为与血管并发症发生相关的 HbA1c 独立危险因素。基于目前对 HbA1c 以及空腹和餐后血糖与糖尿病并发症之间关联的认识,抗糖尿病策略的重点是改善所有这些因素,以降低与糖尿病相关的负担。

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