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糖尿病大血管病变中的氧化应激:同型半胱氨酸起作用吗?

Oxidative stress in diabetic macrovascular disease: does homocysteine play a role?

作者信息

Fonseca V A, Stone A, Munshi M, Baliga B S, Aljada A, Thusu K, Fink L, Dandona P

机构信息

Division of Endocrinology and Metabolism, John L. McClellan Memorial Veterans' Hospital, Little Rock, AR 72205, USA.

出版信息

South Med J. 1997 Sep;90(9):903-6. doi: 10.1097/00007611-199709000-00008.

Abstract

BACKGROUND

Non-insulin-dependent diabetes mellitus (NIDDM) and hyperhomocysteinemia are both associated with increased lipid peroxidation (oxidative stress). This may contribute to the accelerated vascular disease associated with these conditions. It is not known whether the coexistence of elevated homocysteine levels will stimulate oxidative stress further than that caused by diabetes alone.

METHODS

Plasma concentrations of thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, were measured in patients with NIDDM who had previously had a methionine load test; some of the patients had hyperhomocysteinemia.

RESULTS

Plasma TBARS concentrations were elevated in diabetics with vascular disease. The additional presence of hyperhomocysteinemia was not associated with a further increase in plasma TBARS concentrations.

CONCLUSIONS

Lipid peroxidation is increased in patients with diabetes mellitus and macrovascular disease and is not further elevated by the coexistence of elevated homocysteine levels. It is possible that diabetes maximally stimulates oxidative stress and any further acceleration of vascular disease in patients who have coexistent hyperhomocysteinemia is mediated through mechanisms other than lipid peroxidation.

摘要

背景

非胰岛素依赖型糖尿病(NIDDM)和高同型半胱氨酸血症均与脂质过氧化(氧化应激)增加有关。这可能导致与这些病症相关的血管疾病加速发展。目前尚不清楚同型半胱氨酸水平升高与糖尿病单独引起的氧化应激相比,是否会进一步刺激氧化应激。

方法

对之前进行过蛋氨酸负荷试验的NIDDM患者测定血浆中硫代巴比妥酸反应性物质(TBARS)的浓度,TBARS是脂质过氧化的一个指标;部分患者存在高同型半胱氨酸血症。

结果

患有血管疾病的糖尿病患者血浆TBARS浓度升高。高同型半胱氨酸血症的额外存在与血浆TBARS浓度的进一步升高无关。

结论

糖尿病和大血管疾病患者的脂质过氧化增加,且同型半胱氨酸水平升高并不会使其进一步升高。糖尿病可能最大程度地刺激氧化应激,而对于同时存在高同型半胱氨酸血症的患者,血管疾病的任何进一步加速都是通过脂质过氧化以外的机制介导的。

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