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N-乙酰半胱氨酸能够降低2型糖尿病患者高糖饮食后的氧化状态和内皮激活。

N-acetylcysteine is able to reduce the oxidation status and the endothelial activation after a high-glucose content meal in patients with Type 2 diabetes mellitus.

作者信息

Masha A, Brocato L, Dinatale S, Mascia C, Biasi F, Martina V

机构信息

Department of Internal Medicine, Division of Endocrinology, University of Turin, Corso A.M. Dogliotti 14, 10126 Turin, Italy.

出版信息

J Endocrinol Invest. 2009 Apr;32(4):352-6. doi: 10.1007/BF03345726.

DOI:10.1007/BF03345726
PMID:19636205
Abstract

UNLABELLED

Post-prandial hyperglycemia seems to play a pivotal role in the pathogenesis of the cardiovascular complications of diabetes mellitus, as it leads to an oxidative stress which in turn causes a reduced NO bioavailability. These conditions produce an endothelial activation.

AIM OF THE STUDY

The aim of this study was to assure that the administration of N-acetylcysteine (NAC), thiolic antioxidant, is able to decrease the oxidation status and endothelial activation after a high-glucose content meal.

SUBJECTS AND METHODS

Ten patients with Type 2 diabetes mellitus (DMT2) (Group 1) and 10 normal subjects (Group 2) were studied. They assumed a high-glucose content meal without (phase A) or after (phase B) the administration of NAC. Glycemia, insulinemia, intercellular adhesion molecule 1, vascular adhesion molecule 1 (VCAM-1), E-selectin, malonaldehyde (MDA), and 4-hydroxynonenal (HNE) were assessed at -30, 0, +30, +60, +90, +120, and +180 min with respect to the meal consumption.

RESULTS

During the phase A in Group 1, only HNE and MDA levels increased after the meal assumption; all parameters remained unchanged in Group 2. During the phase B, in Group 1, HNE, MDA, VCAM-1, and E-selectin levels after the meal were lower than those in phase A, while no change for all variables were observed in Group 2.

CONCLUSIONS

A high-glucose meal produces an increase in oxidation parameters in patients with DMT2. The administration of NAC reduces the oxidative stress and, by doing so, reduces the endothelial activation. In conclusion, NAC could be efficacious in the slackening of the progression of vascular damage in DMT2.

摘要

未标注

餐后高血糖似乎在糖尿病心血管并发症的发病机制中起关键作用,因为它会导致氧化应激,进而使一氧化氮生物利用度降低。这些情况会引发内皮细胞激活。

研究目的

本研究的目的是确定给予硫醇类抗氧化剂N-乙酰半胱氨酸(NAC)是否能够降低高糖餐后的氧化状态和内皮细胞激活。

研究对象与方法

对10例2型糖尿病患者(第1组)和10例正常受试者(第2组)进行研究。他们在未服用NAC(A阶段)或服用NAC后(B阶段)摄入高糖餐。在进食后-30、0、+30、+60、+90、+120和+180分钟评估血糖、胰岛素、细胞间黏附分子1、血管细胞黏附分子1(VCAM-1)、E-选择素、丙二醛(MDA)和4-羟基壬烯醛(HNE)。

结果

在第1组的A阶段,餐后仅HNE和MDA水平升高;第2组所有参数均保持不变。在B阶段,第1组餐后HNE、MDA、VCAM-1和E-选择素水平低于A阶段,而第2组所有变量均未观察到变化。

结论

高糖餐会使2型糖尿病患者的氧化参数升高。给予NAC可降低氧化应激,从而减少内皮细胞激活。总之,NAC可能对减缓2型糖尿病血管损伤的进展有效。

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