Progress in the role of oxidative stress in the pathogenesis of type 2 diabetes.
- Author:
Chun-Jiu REN
1
,
2
;
Yao ZHANG
;
Wei-Zheng CUI
;
Zhi-Mei MU
Author Information
1. Laboratory of Sericulture Pathology, School of Forest
2. College of Life Sciences, Shandong Agricultural University, Taian 271018, China. zmeimu@sdau.edu.cn.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Diabetes Mellitus, Type 2;
physiopathology;
Humans;
Insulin;
physiology;
Insulin Resistance;
Mitochondria;
pathology;
NF-kappa B;
metabolism;
Oxidative Stress;
Phosphatidylinositol 3-Kinases;
metabolism;
Phosphorylation;
Reactive Oxygen Species;
metabolism;
Signal Transduction
- From:
Acta Physiologica Sinica
2013;65(6):664-673
- CountryChina
- Language:Chinese
-
Abstract:
Diabetes mellitus (DM) is characterized by hyperglycemia and disturbances of carbohydrate and fat metabolism resulted from an absolute or relative deficiency of insulin and insulin resistance. Recent studies indicate that oxidative stress may have a central role in the pathogenesis of type 2 diabetes. Currently, the diagnosis of body oxidative stress level mainly depends on the detection of oxidative stress markers including reactive oxygen species (ROS), reactive nitrogen species (RNS) and lipid peroxide in clinical and experimental studies with methods combining physical and chemical means. The mechanism underlying oxidative stress-induced diabetes mainly may be through two ways. Firstly oxidative stress damages the normal function of islet β cells, through the destruction of mitochondrial structure and inducing apoptosis, activation of nuclear transcription factor kappa B (NF-κB) signaling pathway, causing cell inflammatory response, and reducing insulin synthesis and secretion by inhibiting pancreatic and duodenal homeobox 1 (PDX-1) nuclear cytoplasm translocation as well as inhibiting energy metabolism; Secondly, oxidative stress induces insulin resistance by interfering physiological activities related to insulin signaling including phosphorylation of insulin receptor (InsR) and insulin receptor substrate (IRS), the activation of phosphatidylinositol 3-kinase (PI3K) and the translocation of glucose transporter 4 (GLUT4), as well as injuring the cytoskeleton. Studying the role of oxidative stress in the pathogenesis of diabetes not only helps to reveal the pathogenesis of diabetes, but also provides a theoretical basis for the prevention and treatment of diabetes.
