당뇨병과 산화 스트레스 미토콘드리아 및 NAD(P)H Oxidase에 의한 ROS의 생성과 역할

• Published in: Diabetes & metabolism journal Vol. 32; no. 5; pp. 389 - 398
• Main Authors: 김상수, Sang Soo Kim, 손석만, Seok Man Son
• Format: Journal Article
• Language: Korean
• Published: 대한당뇨병학회 30-10-2008
• Subjects: Diabetes; Mitochondria; NAD(P)H oxidiase; Oxidative stress; ROS; 내과학
• ISSN: 2233-6079; 2233-6087

Oxidative stress has been considered to be a major contributor to the pathogenesis of the diabetic macrovascular and microvascular complications. In the absence of an appropriate antioxidant defense mechanism, increased oxidative stress leads to the activation of stress-sensitive intracellular signaling pathways and the formation of gene products that cause damage and contribute to the late complications of diabetes. The source of reactive oxygen species (ROS) in the pancreatic beta cells and insulin sensitive cells has postulated to be the mitochondrial electron transport chain. NAD(P)H oxidase-dependent ROS production is also important as the source both in pancreatic beta cells and other cells. NAD(P)H oxidase mediated ROS can alter parameters of signal transduction, insulin secretion, insulin action, cell proliferation and cell death. Additionally, oxidative stress as the pathogenic mechanism linking insulin resistance with dysfunction of both pancreatic beta cells and endothelial cells, eventually leads to diabetes and its complications. Further investigation of the mechanisms and its therapeutic interventions based on focusing NAD(P)H oxidase associated ROS production in the islet cells and other islet cells are needed.(KOREAN DIABETES J 32:389-398, 2008)