Effects of Glucose Load and Nateglinide Intervention on Endothelial Function and Oxidative Stress

We analysed endothelial function and oxidative stress in patients with abnormal glucose metabolism, the effect of glucose load, and the impact of nateglinide. 109 participants were grouped into newly diagnosed diabetes, prediabetes, and control. Fasting plasma glucose (FPG), postprandial plasma glucose (PPG), glycosylated haemoglobin ( ), and glycated albumin (GA) varied significantly among the study groups ( ). Nitric oxide (NO) and insulin resistance index (HOMA-IRI) levels were markedly different between the newly diagnosed diabetes and the control ( ). Glucose loading lowered flow-mediated endothelium-dependent dilation (FMEDD), NO, and superoxide dismutase (SOD) ( ). Fasting and glucose loading FMEDD, FPG, PPG, , and GA were negatively correlated ( , ？0.4602, ？0.3895, ？0.3897, and , ？0.4803, ？0.4494, ？0.3885; ), whereas NO, SOD, and HOMA-β were positively correlated ( , 0.3211, 0.311, and , 0.361, 0.2569; ). After the treatment with nateglinide, significant decreases in FPG, PPG, GA, HbA1C, endothelin-1(ET-1), malondialdehyde (MDA), and HOMA-IRI were observed, whereas FMEDD, NO, and SOD increased ( ). Thus, the study demonstrated the adverse effect of glucose load on endothelial function and oxidative stress. Nateglinide lowers blood glucose, reduces insulin resistance and oxidative stress, and improves endothelial function in newly diagnosed diabetes. 1. Introduction The incidence of diabetes is increasing at an alarming rate worldwide. The prevalence of diabetes, reported as about 346 million by WHO, is predicted to advance further in the future if not treated [1]. Diabetes, a chronic metabolic disorder characterised by hyperglycaemia and glucose intolerance, is associated with both macrovascular and microvascular complications [2]. Diabetes-induced vascular complications such as cardiovascular, cerebrovascular, and peripheral vascular diseases adversely affect the life expectancy and quality of life of the patients. At the cellular level, endothelial and vascular smooth cell dysfunction along with abnormal coagulation system is associated with the pathogenesis of diabetes-linked vascular complications [3]. Among these factors, vascular endothelial dysfunction is a key pathological factor in promoting diabetic vascular complications. Oxidative stress, one of the major mechanisms responsible for vascular endothelial dysfunction, is mediated through increased reactive oxygen species (ROS). Elevated ROS is generated through diverse biochemical pathways impacted by hyperglycaemic conditions [4]. In normal vascular endothelium, regulatory mediators,