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Mitochondrial proteome analysis reveals altered expression of voltage dependent anion channels in pancreatic beta-cells exposed to high glucose

Ahmed Khandker, Meftun LU ; Jabar Muhammed, Sarheed LU ; Kessler, Benedikt and Salehi, S Albert LU (2010) In Islets 2(5). p.283-292
Abstract
Chronic hyperglycemia leads to deterioration of insulin release from pancreatic beta-cells as well as insulin action on peripheral tissues. However, the mechanism underlying beta-cell dysfunction resulting from glucose toxicity has not been fully elucidated. The aim of the present study was to define a set of alterations in mitochondrial protein profiles of pancreatic beta-cell line in response to glucotoxic condition using 2-DE and tandem mass spectrometry. INS1E cells were incubated in the presence of 5.5 and 20 mM glucose for 72 hrs and mitochondria were isolated. Approximately 75 protein spots displayed significant changes (p < 0.05) in relative abundance in the presence of 20 mM glucose compared to controls. Mitochondrial proteins... (More)
Chronic hyperglycemia leads to deterioration of insulin release from pancreatic beta-cells as well as insulin action on peripheral tissues. However, the mechanism underlying beta-cell dysfunction resulting from glucose toxicity has not been fully elucidated. The aim of the present study was to define a set of alterations in mitochondrial protein profiles of pancreatic beta-cell line in response to glucotoxic condition using 2-DE and tandem mass spectrometry. INS1E cells were incubated in the presence of 5.5 and 20 mM glucose for 72 hrs and mitochondria were isolated. Approximately 75 protein spots displayed significant changes (p < 0.05) in relative abundance in the presence of 20 mM glucose compared to controls. Mitochondrial proteins downregulated under glucotoxic conditions includes ATP synthase a chain and delta chain, malate dehydrogenase, aconitase, trifunctional enzyme beta subunit, NADH-cytochrome b5 reductase and voltage-dependent anion-selective channel protein (VDAC) 2. VDAC 1, 75 kDa glucose-regulated protein, heat shock protein (HSP) 60 and HSP10 were found to be upregulated. The orchestrated changes in expression of VDACs and multiple other proteins involved in nutrient metabolism, ATP synthesis, cellular defense, glycoprotein folding and mitochondrial DNA stability may explain cellular dysfunction in glucotoxicity resulting in altered insulin secretion. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
proteomics, two-dimensional gel electrophoresis, voltage-dependent, anion-selective channel proteins, mitochondria, insulin secretion, mass, spectrometry
in
Islets
volume
2
issue
5
pages
283 - 292
publisher
Landes Bioscience
external identifiers
  • wos:000289688900004
ISSN
1938-2022
DOI
10.4161/isl.2.5.12639
language
English
LU publication?
yes
id
23e99724-8fe6-4722-acbe-90128aa66b8d (old id 1963969)
date added to LUP
2011-05-20 10:58:43
date last changed
2018-05-29 12:31:49
@article{23e99724-8fe6-4722-acbe-90128aa66b8d,
  abstract     = {Chronic hyperglycemia leads to deterioration of insulin release from pancreatic beta-cells as well as insulin action on peripheral tissues. However, the mechanism underlying beta-cell dysfunction resulting from glucose toxicity has not been fully elucidated. The aim of the present study was to define a set of alterations in mitochondrial protein profiles of pancreatic beta-cell line in response to glucotoxic condition using 2-DE and tandem mass spectrometry. INS1E cells were incubated in the presence of 5.5 and 20 mM glucose for 72 hrs and mitochondria were isolated. Approximately 75 protein spots displayed significant changes (p &lt; 0.05) in relative abundance in the presence of 20 mM glucose compared to controls. Mitochondrial proteins downregulated under glucotoxic conditions includes ATP synthase a chain and delta chain, malate dehydrogenase, aconitase, trifunctional enzyme beta subunit, NADH-cytochrome b5 reductase and voltage-dependent anion-selective channel protein (VDAC) 2. VDAC 1, 75 kDa glucose-regulated protein, heat shock protein (HSP) 60 and HSP10 were found to be upregulated. The orchestrated changes in expression of VDACs and multiple other proteins involved in nutrient metabolism, ATP synthesis, cellular defense, glycoprotein folding and mitochondrial DNA stability may explain cellular dysfunction in glucotoxicity resulting in altered insulin secretion.},
  author       = {Ahmed Khandker, Meftun and Jabar Muhammed, Sarheed and Kessler, Benedikt and Salehi, S Albert},
  issn         = {1938-2022},
  keyword      = {proteomics,two-dimensional gel electrophoresis,voltage-dependent,anion-selective channel proteins,mitochondria,insulin secretion,mass,spectrometry},
  language     = {eng},
  number       = {5},
  pages        = {283--292},
  publisher    = {Landes Bioscience},
  series       = {Islets},
  title        = {Mitochondrial proteome analysis reveals altered expression of voltage dependent anion channels in pancreatic beta-cells exposed to high glucose},
  url          = {http://dx.doi.org/10.4161/isl.2.5.12639},
  volume       = {2},
  year         = {2010},
}