Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs
Joint Authors
Bo, Jinshuang
Xie, Shiya
Guo, Yi
Zhang, Chunli
Guan, Yanming
Li, Chunmei
Lu, Jianxin
Meng, Qing H.
Source
Issue
Vol. 2016, Issue 2016 (31 Dec. 2016), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-12-07
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
Methylglyoxal (MG) is a highly reactive glucose metabolic intermediate and a major precursor of advanced glycation end products.
MG level is elevated in hyperglycemic disorders such as diabetes mellitus.
Substantial evidence has shown that MG is involved in the pathogenesis of diabetes and diabetic complications.
We investigated the impact of MG on insulin secretion by MIN6 and INS-1 cells and the potential mechanisms of this effect.
Our study demonstrates that MG impaired insulin secretion by MIN6 or ISN-1 cells in a dose-dependent manner.
It increased reactive oxygen species (ROS) production and apoptosis rate in MIN6 or ISN-1 cells and inhibited mitochondrial membrane potential (MMP) and ATP production.
Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.
These effects of MG were attenuated by MG scavenger N-acetyl cysteine.
Collectively, these data indicate that MG impairs insulin secretion of pancreatic β-cells through increasing ROS production.
High levels of ROS can damage β-cells directly via JNK/P38 upregulation and through activation of UCP2 resulting in reduced MMP and ATP production, leading to β-cell dysfunction and impairment of insulin production.
American Psychological Association (APA)
Bo, Jinshuang& Xie, Shiya& Guo, Yi& Zhang, Chunli& Guan, Yanming& Li, Chunmei…[et al.]. 2015. Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs. Journal of Diabetes Research،Vol. 2016, no. 2016, pp.1-14.
https://search.emarefa.net/detail/BIM-1107997
Modern Language Association (MLA)
Bo, Jinshuang…[et al.]. Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs. Journal of Diabetes Research No. 2016 (2016), pp.1-14.
https://search.emarefa.net/detail/BIM-1107997
American Medical Association (AMA)
Bo, Jinshuang& Xie, Shiya& Guo, Yi& Zhang, Chunli& Guan, Yanming& Li, Chunmei…[et al.]. Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs. Journal of Diabetes Research. 2015. Vol. 2016, no. 2016, pp.1-14.
https://search.emarefa.net/detail/BIM-1107997
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1107997