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目的观察从糖耐量正常、糖耐量受损(IGT)至糖尿病(DM)发展过程中血清丙二醛(MDA)、超氧化物歧化酶(SOD)和血清可溶性细胞间黏附因子-1(sICAM-1)、可溶性血管细胞黏附因子-1(sVCAM-1)的变化,探讨其致糖尿病早期动脉硬化的机制。方法 93例初诊患者,其中糖耐量正常(NGT)组30例,IGT组28例,2型糖尿病(T2DM)组35例,测定MDA、SOD、sICAM-1和sVCAM-1及超声检测颈动脉内膜中层厚度。结果从糖耐量正常、糖耐量受损至糖尿病,随着糖代谢异常的加重,颈动脉内膜中层逐渐增厚,MDA、sICAM-1和sVCAM-1逐渐升高,血SOD逐渐降低(P<0.05)。颈动脉IMT与血清MDA、sICAM-1、sVCAM-1呈正相关,与血清SOD呈负相关;血清sICAM-1、sVCAM-1和MDA呈正相关,与SOD呈负相关。结论糖代谢异常早期即有氧化应激发生并导致了血管内皮损伤,其机制可能和血中sICAM-1与sVCAM-1升高所导致的糖代谢异常患者血管内皮细胞损伤有关。
Objective To observe the changes of serum malondialdehyde (MDA), superoxide dismutase (SOD) and serum soluble intercellular adhesion molecule-1 (sICAM-1) during the development of impaired glucose tolerance (IGT) 1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), and to explore the mechanism of early arteriosclerosis induced by diabetes. Methods Ninety-three newly diagnosed patients, including 30 with normal glucose tolerance (NGT) group, 28 with IGT group and 35 with type 2 diabetes mellitus (T2DM), were detected for MDA, SOD, sICAM-1 and sVCAM- Membrane thickness. Results From normal glucose tolerance and impaired glucose tolerance to diabetes mellitus, the carotid intima-media middle thickening gradually increased with the increase of glucose metabolism abnormality. The levels of MDA, sICAM-1 and sVCAM-1 gradually increased and the blood SOD decreased gradually (P < 0.05). Carotid artery IMT was positively correlated with serum MDA, sICAM-1 and sVCAM-1, but negatively correlated with serum SOD. Serum sICAM-1, sVCAM-1 and MDA were positively correlated with SOD and negatively correlated with serum. Conclusion The early stage of abnormal glucose metabolism may induce oxidative stress and lead to vascular endothelial injury. The mechanism may be related to the damage of vascular endothelial cells in patients with abnormal glucose metabolism due to the increase of sICAM-1 and sVCAM-1 in blood.