BACKGROUND Excessive reactive oxygen species from endothelial mitochondria in type 2 diabetes individuals (T2DM) may occur through multiple related mechanisms, including production of mitochondrial reactive oxygen species (mtROS), inner mitochondrial membrane (Δψm) hyperpolarization, changes in mitochondrial mass and membrane composition, and fission of the mitochondrial networks. Inner mitochondrial membrane proteins uncoupling protein-2 (UCP2) and prohibitin (PHB) can favorably impact mtROS and mitochondrial membrane potential (Δψm). Circulating levels of UCP2 and PHB could potentially serve as biomarker surrogates for vascular health in patients with and without T2DM. METHODS Plasma samples and data from a total of 107 individuals with (N = 52) and without T2DM (N = 55) were included in this study. Brachial artery flow mediated dilation (FMD) was measured by ultrasound. ELISA was performed to measure serum concentrations of PHB1 and UCP2. Mitochondrial membrane potential was measured from isolated leukocytes using JC-1 dye. RESULTS Serum UCP2 levels were significantly lower in T2DM subjects compared to control subjects (3.01 ± 0.34 vs. 4.11 ± 0.41 ng/mL, P = 0.04). There were no significant differences in levels of serum PHB. UCP2 levels significantly and positively correlated with FMDmm (r = 0.30, P = 0.03) in T2DM subjects only and remained significant after multivariable adjustment. Within T2DM subjects, serum PHB levels were significantly and negatively correlated with UCP2 levels (ρ = - 0.35, P = 0.03). CONCLUSION Circulating UCP2 levels are lower in T2DM patients and correlate with endothelium-dependent vasodilation in conduit vessels. UCP2 could be biomarker surrogate for overall vascular health in patients with T2DM and merits additional investigation.

中文翻译：

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在2型糖尿病患者中，线粒体解偶联蛋白2（而非抑制素）的循环水平较低，并且与肱动脉血流介导的扩张相关。

背景2型糖尿病患者（T2DM）的内皮细胞线粒体中过量的活性氧可能通过多种相关机制发生，包括线粒体活性氧（mtROS）的产生，线粒体内膜（Δψm）超极化，线粒体质量和膜组成的变化，线粒体网络的裂变 线粒体内膜蛋白解偶联蛋白2（UCP2）和禁止素（PHB）可以有利地影响mtROS和线粒体膜电位（Δψm）。患有和不患有T2DM的患者，循环中的UCP2和PHB的水平可能会成为血管健康的生物标志物替代指标。方法这项研究包括来自107名有（N = 52）和没有T2DM（N = 55）的个体的血浆样本和数据。通过超声测量肱动脉血流介导的扩张（FMD）。进行ELISA以测量PHB1和UCP2的血清浓度。使用JC-1染料从分离的白细胞中测定线粒体膜电位。结果与对照组相比，T2DM受试者的血清UCP2水平显着降低（3.01±0.34 vs. 4.11±0.41 ng / mL，P = 0.04）。血清PHB水平无显着差异。仅在T2DM受试者中，UCP2水平与FMDmm呈显着正相关（r = 0.30，P = 0.03），并且在进行多变量调整后仍保持显着水平。在T2DM受试者中，血清PHB水平与UCP2水平显着负相关（ρ=-0.35，P = 0.03）。结论T2DM患者的循环UCP2水平较低，并且与导管血管内皮依赖性血管舒张相关。UCP2可能是T2DM患者总体血管健康的生物标志物替代物，值得进一步研究。