Ascorbic acid treatment and insulin stimulation reduced high glucose-induced ROS production and mitochondrial dysfunction in adipocytes

• Main Authors: Huang, Ching-Yu, 黃晴瑜
• Other Authors: 徐瑞洲
• Format: Others
• Language: zh-TW
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/43670102665049347321

碩士 === 國立清華大學 === 分子醫學研究所 === 102 === Insulin resistance is a characteristic feature of type 2 diabetes mellitus (T2DM) and is accompanied many pathological factors, such as increased oxidative stress and mitochondrial dysfunction. Some studies evidenced that reactive oxygen species (ROS) and mitochondrial dysfunction are involving in the pathological progress, but the molecular mechanisms are still unclear. Glucose transporter 10 (GLUT10) is a member of class III glucose transporter family and encoded by SLC2A10 gene which is located on chromosome 20q12-13.1 where was an association with type 2 diabetes. Previously, our lab has reported that GLUT10 transfers to mitochondrial under insulin stimulation in adipocytes where the GLUT10 is largely expressed. In addition, GLUT10 transports L-dehydroascorbic acid (DHA) in to mitochondria and against oxidative stress under H202-induced stress condition. In this study, we aim to understand the association between GLUT10 and T2DM. We mimic hyperglycemic condition using high glucose treating adipocytes. The treatment leads to increase ROS stress, collapse mitochondrial membrane potential, and decrease oxygen consumption rate. In addition, we found that replenishment with ascorbic acid can not only reduce the intracellular ROS production, but also increase mitochondrial function in adipocytes. Furthermore, treated these adipocytes with insulin can further improve ROS stress and mitochondrial function. My results provide a high glucose stress condition to study the correlation between GLUT10 and insulin resistance in adipocytes.