Delibas Namik, Kilinc Ibrahim, Yonden Zafer, Sutcu Recep, Gultekin Fatih, Koylu Halis
Suleyman Demirel University, Faculty of Medicine, Department of Biochemistry and Physiology, Isparta, Turkey.
Int J Neurosci. 2004 Mar;114(3):391-401. doi: 10.1080/00207450490270893.
Recent studies indicate that diabetes mellitus changes N-methyl-D-aspartate (NMDA) receptor subunit composition and impairs cognitive functions. It also has been known that diabetes mellitus causes lipid peroxidation. This study examined the effects of streptozotocin-diabetes and insulin or gliclazide treatment on the hippocampal NMDA receptor subunit 2A and 2B (NR2A and NR2B) concentrations. In addition, malondial dehyde (MDA) levels were measured as a marker for lipid peroxidation. Eight weeks after the induction of diabetes MDA, levels were increased, and NR2A and NR2B concentrations were reduced. Insulin and gliclazide treatment partially prevented the reduction of NR2A and NR2B expression and prevented the elevation of MDA levels. There was no significant difference between the effects of insulin and gliclazide. The results suggest that the elevation of lipid peroxidation can be the primary biochemical disturbances in diabetes progression, and that changes in NMDA receptor subunit compositions can be involved in cognitive decline in diabetes.
近期研究表明，糖尿病会改变N-甲基-D-天冬氨酸（NMDA）受体亚基组成，并损害认知功能。众所周知，糖尿病还会导致脂质过氧化。本研究检测了链脲佐菌素诱导的糖尿病以及胰岛素或格列齐特治疗对海马体NMDA受体亚基2A和2B（NR2A和NR2B）浓度的影响。此外，还测量了丙二醛（MDA）水平作为脂质过氧化的标志物。糖尿病诱导八周后，MDA水平升高，NR2A和NR2B浓度降低。胰岛素和格列齐特治疗部分阻止了NR2A和NR2B表达的降低，并阻止了MDA水平的升高。胰岛素和格列齐特的效果之间没有显著差异。结果表明，脂质过氧化的升高可能是糖尿病进展过程中的主要生化紊乱，并且NMDA受体亚基组成的变化可能与糖尿病患者的认知衰退有关。
