Pancreatic islet β-cell and oxidative stress:: The importance of glutathione peroxidase

被引:144
作者
Robertson, R. Paul [1 ]
Harmon, Jamie S. [1 ]
机构
[1] Univ Washington, Pacific NW Res Inst, Seattle, WA 98122 USA
来源
FEBS LETTERS | 2007年 / 581卷 / 19期
关键词
type; 2; diabetes; gluathione peroxidase; pancreatic; beta-cell;
D O I
10.1016/j.febslet.2007.03.087
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pancreatic beta-cell function continuously deteriorates in type 2 diabetes despite optimal treatment regimens, which has been attributed to hyperglycemia itself via formation of excess levels of reactive oxygen species (ROS). Glutathione peroxidase GPx), by virtue of its ability to catabolize both H2O2 and lipid peroxides, is uniquely positioned to protect tissues from ROS. The level of this antioxidant in 0 cells is extremely low and overexpression of GPx in islets provides enhanced protection against oxidative stress. This suggests that GPx mimetics may represent a valuable ancillary treatment that could add a novel layer of protection for the P-cell. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3743 / 3748
页数:6
相关论文
共 43 条
  • [1] Long-term exposure of isolated rat islets of langerhans to supraphysiologic glucose concentrations decreases insulin mRNA levels
    Briaud, I
    Rouault, C
    Reach, G
    Poitout, V
    [J]. METABOLISM-CLINICAL AND EXPERIMENTAL, 1999, 48 (03): : 319 - 323
  • [2] Differential effects of hyperlipidemia on insulin secretion in islets of Langerhans from hyperglycemic versus normoglycemic rats
    Briaud, I
    Kelpe, CL
    Johnson, LM
    Tran, POT
    Poitout, V
    [J]. DIABETES, 2002, 51 (03) : 662 - 668
  • [3] Lipotoxicity of the pancreatic β-cell is associated with glucose-dependent esterification of fatty acids into neutral lipids
    Briaud, I
    Harmon, JS
    Kelpe, CL
    Segu, VBG
    Poitout, V
    [J]. DIABETES, 2001, 50 (02) : 315 - 321
  • [4] Glucose-induced oxidative stress in mesangial cells
    Catherwood, MA
    Powell, LA
    Anderson, P
    McMaster, D
    Sharpe, PC
    Trimble, ER
    [J]. KIDNEY INTERNATIONAL, 2002, 61 (02) : 599 - 608
  • [5] SALICYLATE HYDROXYLATION AS AN EARLY MARKER OF INVIVO OXIDATIVE STRESS IN DIABETIC-PATIENTS
    GHISELLI, A
    LAURENTI, O
    DEMATTIA, G
    MAIANI, G
    FERROLUZZI, A
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1992, 13 (06) : 621 - 626
  • [6] PLASMA 8-EPI-PGF(2-ALPHA) LEVELS ARE ELEVATED IN INDIVIDUALS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS
    GOPAUL, NK
    ANGGARD, EE
    MALLET, AI
    BETTERIDGE, DJ
    WOLFF, SP
    NOUROOZZADEH, J
    [J]. FEBS LETTERS, 1995, 368 (02) : 225 - 229
  • [7] CUZN-SUPEROXIDE DISMUTASE, MN-SUPEROXIDE DISMUTASE, CATALASE AND GLUTATHIONE-PEROXIDASE IN PANCREATIC-ISLETS AND OTHER TISSUES IN THE MOUSE
    GRANKVIST, K
    MARKLUND, SL
    TALJEDAL, IB
    [J]. BIOCHEMICAL JOURNAL, 1981, 199 (02) : 393 - 398
  • [8] Fatty acids decrease IDX-1 expression in rat pancreatic islets and reduce GLUT2, glucokinase, insulin, and somatostatin levels
    Gremlich, S
    Bonny, C
    Waeber, G
    Thorens, B
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (48) : 30261 - 30269
  • [9] In vivo prevention of hyperglycemia also prevents glucotoxic effects on PDX-1 and insulin gene expression
    Harmon, JS
    Gleason, CE
    Tanaka, Y
    Oseid, EA
    Hunter-Berger, KK
    Robertson, RP
    [J]. DIABETES, 1999, 48 (10) : 1995 - 2000
  • [10] Oxidative stress-mediated, post-translational loss of MafA protein as a contributing mechanism to loss of insulin gene expression in glucotoxic beta cells
    Harmon, JS
    Stein, R
    Robertson, RP
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (12) : 11107 - 11113