Wright E, Scism-Bacon J L, Glass L C
Primary Care and Specialty Practices of Cape Fear Valley Health System, Cape Fear Valley Health System, Fayetteville, NC 28302, USA.
Int J Clin Pract. 2006 Mar;60(3):308-14. doi: 10.1111/j.1368-5031.2006.00825.x.
Oxidative stress, through the production of reactive oxygen species (ROS), has been proposed as the root cause underlying the development of insulin resistance, beta-cell dysfunction, impaired glucose tolerance and type 2 diabetes mellitus (T2DM). It has also been implicated in the progression of long-term diabetes complications, including microvascular and macrovascular dysfunction. Excess nourishment and a sedentary lifestyle leads to glucose and fatty acid overload, resulting in production of ROS. Additionally, reaction of glucose with plasma proteins forms advanced glycation end products, triggering production of ROS. These ROS initiate a chain reaction leading to reduced nitric oxide availability, increased markers of inflammation and chemical modification of lipoproteins, all of which may increase the risk of atherogenesis. With the postulation that hyperglycaemia and fluctuations in blood glucose lead to generation of ROS, it follows that aggressive treatment of fasting and postprandial hyperglycaemia is important for prevention of micro and macrovascular complications in T2DM.
氧化应激通过产生活性氧（ROS），被认为是胰岛素抵抗、β细胞功能障碍、糖耐量受损和2型糖尿病（T2DM）发生发展的根本原因。它还与糖尿病长期并发症的进展有关，包括微血管和大血管功能障碍。营养过剩和久坐不动的生活方式会导致葡萄糖和脂肪酸过载，从而产生活性氧。此外，葡萄糖与血浆蛋白反应形成晚期糖基化终产物，引发活性氧的产生。这些活性氧引发连锁反应，导致一氧化氮可用性降低、炎症标志物增加以及脂蛋白的化学修饰，所有这些都可能增加动脉粥样硬化的风险。基于高血糖和血糖波动会导致活性氧生成的假设，积极治疗空腹和餐后高血糖对于预防T2DM的微血管和大血管并发症很重要。
