Glucotoxicity and pancreatic proteomics

被引:46
作者
Brunner, Yannick [1 ]
Schvartz, Domitille [1 ]
Priego-Capote, Feliciano [1 ]
Coute, Yohann [1 ]
Sanchez, Jean-Charles [1 ]
机构
[1] CMU, Biomed Proteom Res Grp, DBSB, CH-1211 Geneva 4, Switzerland
关键词
Diabetes; Glucotoxicity; Proteomics; Mass spectrometry; ENDOPLASMIC-RETICULUM STRESS; GLYCATION END-PRODUCTS; BETA-CELL APOPTOSIS; 2-DIMENSIONAL GEL-ELECTROPHORESIS; INSULIN GENE-TRANSCRIPTION; NON ENZYMATIC GLYCATION; APOLIPOPROTEIN-A-I; ALPHA-LIPOIC ACID; OXIDATIVE STRESS; HIGH GLUCOSE;
D O I
10.1016/j.jprot.2008.10.002
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Chronic hyperglycaemia. is one of the main characteristics of a diabetic state. This is also the first cause of diabetic complications. However, it is now generally accepted that glucotoxicity also participates in the worsening of type 2 diabetes, by affecting the secretion of beta-cells. So far, different mechanisms have been proposed to explain the adverse effects of chronic hyperglycaemia. One of them suggests that the modulation of expression of several key proteins during a hyperglycaemia state, may explain the toxic effect of glucotoxicity. Therefore, proteomic analysis of biological samples represents an interesting method to study the effect of chronic hyperglycaemia on protein expression. The discovery of new proteins for which the expression could be modulated by chronic hyperglycaemia may probably help to better understand the mechanisms underlying glucotoxicity. In this review, we will first present an introduction of the different mechanisms known to be involved in the control of glucose homeostasis and in the development of glucotoxicity. in a second part, some proteomic data linked with the effect of glucotoxicity in pancreas, pancreatic islets and beta-cells will be presented and discussed. (C) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:576 / 591
页数:16
相关论文
共 191 条
[21]   MODIFICATION OF LOW-DENSITY-LIPOPROTEIN BY ADVANCED GLYCATION END-PRODUCTS CONTRIBUTES TO THE DYSLIPIDEMIA OF DIABETES AND RENAL-INSUFFICIENCY [J].
BUCALA, R ;
MAKITA, Z ;
VEGA, G ;
GRUNDY, S ;
KOSCHINSKY, T ;
CERAMI, A ;
VLASSARA, H .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (20) :9441-9445
[22]   INSULIN-INHIBITION OF LIPOLYSIS OF HUMAN ADIPOCYTES - ROLE OF CYCLIC ADENOSINE-MONOPHOSPHATE [J].
BURNS, TW ;
TERRY, BE ;
LANGLEY, PE ;
ROBISON, GA .
DIABETES, 1979, 28 (11) :957-961
[23]  
CALVO C, 1988, DIABETES METAB, V14, P264
[24]   NON ENZYMATIC GLYCATION OF APOLIPOPROTEIN-A-I - EFFECTS ON ITS SELF-ASSOCIATION AND LIPID-BINDING PROPERTIES [J].
CALVO, C ;
TALUSSOT, C ;
PONSIN, G ;
BERTHEZENE, F .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1988, 153 (03) :1060-1067
[25]  
CALVO C, 1992, EUR J CLIN CHEM CLIN, V30, P3
[26]   Intra-islet somatostatin regulates glucagon release via type 2 somatostatin receptors in rats [J].
Cejvan, K ;
Coy, DH ;
Efendic, S .
DIABETES, 2003, 52 (05) :1176-1181
[27]   The Rab-binding protein Noc2 is associated with insulin-containing secretory granules and is essential for pancreatic β-cell exocytosis [J].
Cheviet, S ;
Coppola, T ;
Haynes, LP ;
Burgoyne, RD ;
Regazzi, R .
MOLECULAR ENDOCRINOLOGY, 2004, 18 (01) :117-126
[28]   Tomosyn-1 is involved in a post-docking event required for pancreatic β-cell exocytosis [J].
Cheviet, Severine ;
Bezzi, Paola ;
Ivarsson, Rosita ;
Renstrom, Erik ;
Viertl, David ;
Kasas, Sandor ;
Catsicas, Stefan ;
Regazzi, Romano .
JOURNAL OF CELL SCIENCE, 2006, 119 (14) :2912-2920
[29]   THE ACUTE EFFECT OF FAT ON INSULIN-SECRETION [J].
COLLIER, GR ;
GREENBERG, GR ;
WOLEVER, TMS ;
JENKINS, DJA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1988, 66 (02) :323-326
[30]   Pancreatic β-cell protein granuphilin binds Rab3 and Munc-18 and controls exocytosis [J].
Coppola, T ;
Frantz, C ;
Perret-Menoud, V ;
Gattesco, S ;
Hirling, H ;
Regazzi, R .
MOLECULAR BIOLOGY OF THE CELL, 2002, 13 (06) :1906-1915