Asymmetric dimethylarginine is an endogenous competitive inhibitor of nitric oxide synthase and marker of endothelial dysfunction, but the question remains as to whether asymmetric dimethylarginine is a marker of cardiovascular episodes or their independent risk factor. ADMA/DDAH (dimethylaminohydrolase) pathway regulates vascular endothelial growth factor (VEGF)-mediated angiogenesis due to its impact on the NO formation. The aim of the study was to assess the concentrations of asymmetric dimethylarginine and the angiogenic potential in the blood of subjects with type 2 diabetes (T2DM, n = 33) and patients with prediabetes (n = 32)—impaired fasting glycemia and/or impaired glucose tolerance (WHO criteria). The study found that both the prediabetes group and subjects with T2DM had significantly elevated concentrations of asymmetric dimethylarginine, significantly high levels of VEGF-A, low ratio of sVEGF-R1/VEGF-A, and sVEGF-R2/VEGF-A. This may suggest endothelial damage at early stages of carbohydrate metabolism dysfunction—before T2DM is diagnosed. Higher proangiogenic potential in prediabetes and T2DM patients than in healthy subjects, is not only the effect of an increase in VEGF-A levels, but also reduced inhibition of circulating receptors.

Impact statement

Our research provided new insight into the mechanisms governing vascular complications in prediabetes and type 2 diabetes. Unfortunately, most studies focus on angiogenesis markers (VEGF-A, sVEGF-R1, sVEGF-R2) and endothelial dysfunction marker (ADMA) separately. Our findings reported for the first time that endothelial damage and angiogenic potential at early stage of carbohydrate dysfunction appear in prediabetes before type 2 diabetes is diagnosed.

中文翻译：

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ADMA（不对称二甲基精氨酸）和 2 型糖尿病和糖尿病前期患者的血管生成潜力。

不对称二甲基精氨酸是一氧化氮合酶的内源性竞争性抑制剂和内皮功能障碍的标志物，但问题仍然是不对称二甲基精氨酸是心血管事件的标志物还是心血管事件的独立危险因素。ADMA/DDAH（二甲氨基水解酶）途径由于其对 NO 形成的影响而调节血管内皮生长因子 (VEGF) 介导的血管生成。该研究的目的是评估非对称二甲基的浓度和在2型糖尿病的受试者的血液中的血管生成潜力（T2DM，Ñ  = 33）和患有前驱糖尿病（Ñ = 32)——空腹血糖受损和/或糖耐量受损（WHO 标准）。研究发现，糖尿病前期组和 T2DM 受试者的不对称二甲基精氨酸浓度显着升高，VEGF-A 水平显着升高，sVEGF-R1/VEGF-A 和 sVEGF-R2/VEGF-A 的比率较低。这可能表明在碳水化合物代谢功能障碍的早期阶段（在诊断出 T2DM 之前）内皮损伤。与健康受试者相比，糖尿病前期和 T2DM 患者具有更高的促血管生成潜力，这不仅是 VEGF-A 水平增加的影响，而且还降低了对循环受体的抑制。

影响陈述

我们的研究为控制糖尿病前期和 2 型糖尿病血管并发症的机制提供了新的见解。不幸的是，大多数研究分别关注血管生成标志物（VEGF-A、sVEGF-R1、sVEGF-R2）和内皮功能障碍标志物（ADMA）。我们的研究结果首次报道，在诊断出 2 型糖尿病之前，糖尿病前期就出现了碳水化合物功能障碍早期的内皮损伤和血管生成潜力。