辅酶Q(10)可改善II型糖尿病患者肱动脉的内皮功能障碍。

Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus.

作者信息

Watts G F, Playford D A, Croft K D, Ward N C, Mori T A, Burke V

机构信息

Department of Medicine, University of Western Australia, Royal Perth Hospital, Perth, Australia.

出版信息

Diabetologia. 2002 Mar;45(3):420-6. doi: 10.1007/s00125-001-0760-y.

DOI:10.1007/s00125-001-0760-y

PMID:11914748

Abstract

AIM/HYPOTHESIS: We assessed whether dietary supplementation with coenzyme Q(10) improves endothelial function of the brachial artery in patients with Type II (non-insulin-dependent) diabetes mellitus and dyslipidaemia.

METHODS

A total of 40 patients with Type II diabetes and dyslipidaemia were randomized to receive 200 mg of coenzyme Q(10) or placebo orally for 12 weeks. Endothelium-dependent and independent function of the brachial artery was measured as flow-mediated dilatation and glyceryl-trinitrate-mediated dilatation, respectively. A computerized system was used to quantitate vessel diameter changes before and after intervention. Arterial function was compared with 18 non-diabetic subjects. Oxidative stress was assessed by measuring plasma F(2)-isoprostane concentrations, and plasma antioxidant status by oxygen radical absorbance capacity.

RESULTS

The diabetic patients had impaired flow-mediated dilation [3.8 % (SEM 0.5) vs 6.4 % (SEM 1.0), p = 0.016], but preserved glyceryl-trinitrate-mediated dilation, of the brachial artery compared with non-diabetic subjects. Flow-mediated dilation of the brachial artery increased by 1.6 % (SEM 0.3) with coenzyme Q(10) and decreased by -0.4 % (SEM 0.5) with placebo (p = 0.005); there were no group differences in the changes in pre-stimulatory arterial diameter, post-ischaemic hyperaemia or glyceryl-trinitrate-mediated dilation response. Coenzyme Q(10) treatment resulted in a threefold increase in plasma coenzyme Q(10) (p < 0.001) but did not alter plasma F(2)-isoprostanes, oxygen radical absorbance capacity, lipid concentrations, glycaemic control or blood pressure.

CONCLUSION/INTERPRETATION: Coenzyme Q(10) supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes. The mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress, an effect that might not be reflected by changes in plasma F(2)-isoprostane concentrations.

摘要

目的/假设：我们评估了补充辅酶Q10是否能改善2型（非胰岛素依赖型）糖尿病和血脂异常患者肱动脉的内皮功能。

方法

40例2型糖尿病和血脂异常患者被随机分为两组，分别口服200毫克辅酶Q10或安慰剂，为期12周。肱动脉的内皮依赖性和非依赖性功能分别通过血流介导的扩张和硝酸甘油介导的扩张来测量。使用计算机系统对干预前后的血管直径变化进行定量分析。将动脉功能与18名非糖尿病受试者进行比较。通过测量血浆F2-异前列腺素浓度评估氧化应激，通过氧自由基吸收能力评估血浆抗氧化状态。

结果

与非糖尿病受试者相比，糖尿病患者肱动脉的血流介导的扩张受损[3.8%（标准误0.5）对6.4%（标准误1.0），p = 0.016]，但硝酸甘油介导的扩张保留。辅酶Q10使肱动脉的血流介导的扩张增加了1.6%（标准误0.3），安慰剂使其降低了-0.4%（标准误0.5）（p = 0.005）；刺激前动脉直径、缺血后充血或硝酸甘油介导的扩张反应的变化在两组之间没有差异。辅酶Q10治疗使血浆辅酶Q10增加了三倍（p < 0.001），但未改变血浆F2-异前列腺素、氧自由基吸收能力、血脂浓度、血糖控制或血压。

结论/解读：补充辅酶Q10可改善2型糖尿病血脂异常患者外周循环中传导动脉的内皮功能。其机制可能涉及由于血管氧化应激的改善，内皮释放和/或一氧化氮活性增加，这种作用可能不会通过血浆F2-异前列腺素浓度的变化反映出来。