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Park, Jiyoung
Molecular Metabolism Laboratory (MML)
Research Interests
  • Obesity, diabetes, adipose tissue, cancer, cancer-associated adipocyte, dermal adipocyte, metabolic memory

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G6PD Up-Regulation Promotes Pancreatic beta-Cell Dysfunction

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Title
G6PD Up-Regulation Promotes Pancreatic beta-Cell Dysfunction
Author
Lee, Joo-WonChoi, A. HyunHam, MiraKim, Ji-WonChoe, Sung SikPark, JiyoungLee, Gha YoungYoon, Kun-HoKim, Jae Bum
Keywords
KAPPA-B ACTIVATION;  INSULIN-PRODUCING CELLS;  OXIDATIVE STRESS;  NAD(P)H OXIDASE;  GENE-EXPRESSION;  SUPEROXIDE-PRODUCTION;  GLUCOSE TOXICITY;  CHRONIC EXPOSURE;  GLUCOSE-6-PHOSPHATE-DEHYDROGENASE;  APOPTOSIS
Issue Date
2011-03
Publisher
ENDOCRINE SOC
Citation
ENDOCRINOLOGY, v.152, no.3, pp.793 - 803
Abstract
Increased reactive oxygen species (ROS) induce pancreatic β-cell dysfunction during progressive type 2 diabetes. Glucose-6-phosphate dehydrogenase (G6PD) is a reduced nicotinamide adenine dinucleotide phosphate-producing enzyme that plays a key role in cellular reduction/oxidation regulation. We have investigated whether variations in G6PD contribute to β-cell dysfunction through regulation of ROS accumulation and β-cell gene expression. When the level of G6PD expression in pancreatic islets was examined in several diabetic animal models, such as db/db mice and OLEFT rats, G6PD expression was evidently up-regulated in pancreatic islets in diabetic animals. To investigate the effect of G6PD on β-cell dysfunction, we assessed the levels of cellular ROS, glucose-stimulated insulin secretion and β-cell apoptosis in G6PD-overexpressing pancreatic β-cells. In INS-1 cells, G6PD overexpression augmented ROS accumulation associated with increased expression of prooxidative enzymes, such as inducible nitric oxide synthase and reduced nicotin-amide adenine dinucleotide phosphate oxidase. G6PD up-regulation also caused decrease in glucose-stimulated insulin secretion in INS-1 cells and primary pancreatic islets. Moreover, elevated G6PD expression led to β-cell apoptosis, concomitant with the increase in proapoptotic gene expression. On the contrary, suppression of G6PD with small interference RNA attenuated palmitate-induced β-cell apoptosis. Together, these data suggest that up-regulation of G6PD in pancreatic β-cells would induce β-cell dysregulation through ROS accumulation in the development of type 2 diabetes.
URI
https://scholarworks.unist.ac.kr/handle/201301/7166
DOI
10.1210/en.2010-0606
ISSN
0013-7227
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