Thiazolidinediones and the preservation of β-cell function, cellular proliferation and apoptosis

被引:15
作者
Decker, Michael [1 ]
Hofflich, Heather [1 ]
Elias, Alan N. [1 ]
机构
[1] Univ Calif Irvine, Dept Med, Div Endocrinol Diabet & Metab, Med Ctr, Orange, CA 92868 USA
关键词
anti-inflammatory; apoptosis; beta-cell; diabetes; thiazolidinedione;
D O I
10.1111/j.1463-1326.2007.00745.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The thiazolidinediones (TZDs) or glitazones are pharmaceutical agents that have profound effects on energy expenditure and conservation. They also exert significant anti-inflammatory effects and influence cell proliferation and cell death. The drugs are primarily used in clinical practice in the treatment of patients with type 2 diabetes mellitus, a disorder of insulin resistance that occurs when the pancreatic beta-cells are unable to produce adequate amounts of insulin to maintain euglycaemia. Loss of pancreatic beta-cell function in type 2 diabetes is progressive and often precedes overt diabetes by 10 years or more, as was shown by the United Kingdom Prospective Diabetes Study. Any therapeutic or preventive approach that would limit or reverse loss of beta-cell function in diabetes would have profound effects on the morbidity associated with this widespread disease. Evidence suggesting a potential role of TZDs in preserving beta-cell function in type 2 diabetes as well as the ability of these agents to exert anti-inflammatory and proapoptotic anticancer effects, and their ability to promote cellular proliferation in various organs is reviewed.
引用
收藏
页码:617 / 625
页数:9
相关论文
共 98 条
[1]   The common PPARγ Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes [J].
Altshuler, D ;
Hirschhorn, JN ;
Klannemark, M ;
Lindgren, CM ;
Vohl, MC ;
Nemesh, J ;
Lane, CR ;
Schaffner, SF ;
Bolk, S ;
Brewer, C ;
Tuomi, T ;
Gaudet, D ;
Hudson, TJ ;
Daly, M ;
Groop, L ;
Lander, ES .
NATURE GENETICS, 2000, 26 (01) :76-80
[2]   TRIPOD (TRoglitazone in the Prevention of Diabetes): A randomized, placebo-controlled trial of troglitazone in women with prior gestational diabetes mellitus [J].
Azen, SP ;
Peters, RK ;
Berkowitz, K ;
Kjos, S ;
Xiang, A ;
Buchanan, TA .
CONTROLLED CLINICAL TRIALS, 1998, 19 (02) :217-231
[3]   Therapeutic approaches to preserve islet mass in type 2 diabetes [J].
Baggio, LL ;
Drucker, DJ .
ANNUAL REVIEW OF MEDICINE, 2006, 57 :265-281
[4]   Expression of a dominant negative inhibitor of NF-κB protects MIN6 β-cells from cytokine-induced apoptosis [J].
Baker, MS ;
Chen, XJ ;
Cao, XC ;
Kaufman, DB .
JOURNAL OF SURGICAL RESEARCH, 2001, 97 (02) :117-122
[5]   PPARγ is required for placental, cardiac, and adipose tissue development [J].
Barak, Y ;
Nelson, MC ;
Ong, ES ;
Jones, YZ ;
Ruiz-Lozano, P ;
Chien, KR ;
Koder, A ;
Evans, RM .
MOLECULAR CELL, 1999, 4 (04) :585-595
[6]   β-cell rejuvenation with thiazolidinediones [J].
Bell, DSH .
AMERICAN JOURNAL OF MEDICINE, 2003, 115 :20-23
[7]   Epidermal anti-Inflammatory properties of 5,11,14 20:3: Effects on mouse ear edema, PGE2 levels in cultured keratinocytes, and PPAR activation [J].
Alvin Berger ;
Irina Monnard ;
Markus Baur ;
Corinne Charbonnet ;
Irina Safonova ;
André Jomard .
Lipids in Health and Disease, 1 (1)
[8]   Differential expression of peroxisome proliferator-activated receptors (PPARs): Tissue distribution of PPAR-alpha, -beta, and -gamma in the adult rat [J].
Braissant, O ;
Foufelle, F ;
Scotto, C ;
Dauca, M ;
Wahli, W .
ENDOCRINOLOGY, 1996, 137 (01) :354-366
[9]   Preservation of pancreatic β-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk Hispanic women [J].
Buchanan, TA ;
Xiang, AH ;
Peters, RK ;
Kjos, SL ;
Marroquin, A ;
Goico, J ;
Ochoa, C ;
Tan, S ;
Berkowitz, K ;
Hodis, HN ;
Azen, SP .
DIABETES, 2002, 51 (09) :2796-2803
[10]   β-cell deficit and increased β-cell apoptosis in humans with type 2 diabetes [J].
Butler, AE ;
Janson, J ;
Bonner-Weir, S ;
Ritzel, R ;
Rizza, RA ;
Butler, PC .
DIABETES, 2003, 52 (01) :102-110