Iannantuoni Francesca, M de Marañon Aranzazu, Abad-Jiménez Zaida, Canet Francisco, Díaz-Pozo Pedro, López-Domènech Sandra, Morillas Carlos, Rocha Milagros, Víctor Víctor M
Service of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), 46017 Valencia, Spain.
CIBERehd-Department of Pharmacology and Physiology, University of Valencia, 46010 Valencia, Spain.
J Clin Med. 2020 Jul 8;9(7):2155. doi: 10.3390/jcm9072155.
Type 1 diabetes has been associated with oxidative stress. This study evaluates the rates of oxidative stress, mitochondrial function, leukocyte-endothelium interactions and adhesion molecules in type 1 diabetic patients. The study population consisted of 52 diabetic patients and 46 body-composition and age-matched controls. We assessed anthropometric and metabolic parameters, oxidative stress and mitochondrial function by evaluating reactive oxygen species (ROS) production, mitochondrial ROS production, mitochondrial membrane potential and superoxide dismutase (SOD) and catalase (CAT) expression in polymorphonuclear leukocytes from type 1 diabetic patients. In addition, we evaluated interactions between leukocytes and human umbilical vein endothelial cells (HUVEC), and serum expression of adhesion molecules (P-selectin, VCAM-1 and ICAM-1), proinflammatory cytokines (IL-6 and TNFα) and myeloperoxidase (MPO). HbA and glucose levels were higher in diabetic patients than in control subjects, as expected. Mitochondrial function was altered and leukocyte-endothelium interactions were enhanced in diabetic patients, which was evident in the increase in total and mitochondrial ROS production, higher mitochondrial membrane potential, enhanced leukocyte rolling and adhesion, and decreased rolling velocity. Furthermore, we observed an increase in levels of adhesion molecules P-selectin, VCAM-1, and ICAM-1 in these subjects. In addition, type 1 diabetic patients exhibited an increase in proinflammatory mediators TNFα and MPO, and a decreased expression of SOD. The enhancement of leukocyte-endothelium interactions and proinflammatory markers correlated with glucose and HbAlevels. Mitochondrial alteration, oxidative stress, and enhanced leukocyte-endothelium interactions are features of type 1 diabetes and may be related to cardiovascular implications.
1型糖尿病与氧化应激有关。本研究评估了1型糖尿病患者的氧化应激率、线粒体功能、白细胞与内皮细胞的相互作用及黏附分子。研究对象包括52例糖尿病患者和46例身体成分及年龄匹配的对照者。我们通过评估1型糖尿病患者多形核白细胞中的活性氧（ROS）生成、线粒体ROS生成、线粒体膜电位以及超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的表达，来评估人体测量和代谢参数、氧化应激和线粒体功能。此外，我们评估了白细胞与人类脐静脉内皮细胞（HUVEC）之间的相互作用，以及黏附分子（P-选择素、血管细胞黏附分子-1和细胞间黏附分子-1）、促炎细胞因子（白细胞介素-6和肿瘤坏死因子α）和髓过氧化物酶（MPO）的血清表达。正如预期的那样，糖尿病患者的糖化血红蛋白（HbA）和血糖水平高于对照组。糖尿病患者的线粒体功能发生改变，白细胞与内皮细胞的相互作用增强，这在总ROS和线粒体ROS生成增加、线粒体膜电位升高、白细胞滚动和黏附增强以及滚动速度降低中明显体现。此外，我们观察到这些受试者中黏附分子P-选择素、血管细胞黏附分子-1和细胞间黏附分子-1的水平升高。此外，1型糖尿病患者促炎介质肿瘤坏死因子α和髓过氧化物酶增加，SOD表达降低。白细胞与内皮细胞相互作用及促炎标志物的增强与血糖和HbA水平相关。线粒体改变、氧化应激以及白细胞与内皮细胞相互作用增强是1型糖尿病的特征，可能与心血管方面的影响有关。
