Islet β cell failure in type 2 diabetes

被引:1331
作者
Prentki, Marc
Nolan, Christopher J.
机构
[1] Australian Natl Univ, Dept Endocrinol & Diabet, Canberra Hosp, Woden, ACT 2606, Australia
[2] Australian Natl Univ, Sch Med, Woden, ACT 2606, Australia
[3] Univ Montreal, Mol Nutr Unit, Montreal, PQ, Canada
[4] Univ Montreal, Montreal Diabet Res Ctr, Montreal, PQ, Canada
[5] Ctr Hosp Univ Montreal, Montreal, PQ, Canada
关键词
D O I
10.1172/JCI29103
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The major focus of this Review is on the mechanisms of islet P cell failure in the pathogenesis of obesity-associated type 2 diabetes (T2D). As this demise occurs within the context of P cell compensation for insulin resistance, consideration is also given to the mechanisms involved in the compensation process, including mechanisms for expansion of P cell mass and for enhanced P cell performance. The importance of genetic, intrauterine, and environmental factors in the determination of "susceptible" islets and overall risk for T2D is reviewed. The likely mechanisms of P cell failure are discussed within the two broad categories: those with initiation and those with progression roles.
引用
收藏
页码:1802 / 1812
页数:11
相关论文
共 125 条
[21]  
DelRio G, 1997, INT J OBESITY, V21, P1111
[22]   Structural and functional abnormalities in the islets isolated from type 2 diabetic subjects [J].
Deng, SP ;
Vatamaniuk, M ;
Huang, XL ;
Doliba, N ;
Lian, MM ;
Frank, A ;
Velidedeoglu, E ;
Desai, NM ;
Koeberlein, B ;
Wolf, B ;
Barker, CF ;
Naji, A ;
Matschinsky, FM ;
Markmann, JF .
DIABETES, 2004, 53 (03) :624-632
[23]   A fatty acid-dependent step is critically important for both glucose- and non-glucose-stimulated insulin secretion [J].
Dobbins, RL ;
Chester, MW ;
Stevenson, BE ;
Daniels, MB ;
Stein, DT ;
McGarry, JD .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (11) :2370-2376
[24]   Mechanisms of β-cell death in type 2 diabetes [J].
Donath, MY ;
Ehses, JA ;
Maedler, K ;
Schumann, DM ;
Ellingsgaard, H ;
Eppler, E ;
Reinecke, M .
DIABETES, 2005, 54 :S108-S113
[25]   The biology of incretin hormones [J].
Drucker, DJ .
CELL METABOLISM, 2006, 3 (03) :153-165
[26]  
Du XL, 2003, J CLIN INVEST, V112, P1049, DOI 10.1172/JCI200318127
[27]   Mutation analysis of peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1) and relationships of identified amino acid polymorphisms to Type II diabetes mellitus [J].
Ek, J ;
Andersen, G ;
Urhammer, SA ;
Gæde, PH ;
Drivsholm, T ;
Borch-Johnsen, K ;
Hansen, T ;
Pedersen, O .
DIABETOLOGIA, 2001, 44 (12) :2220-2226
[28]   Saturated fatty acids synergize with elevated glucose to cause pancreatic β-cell death [J].
El-Assaad, W ;
Buteau, J ;
Peyot, ML ;
Nolan, C ;
Roduit, R ;
Hardy, S ;
Joly, E ;
Dbaibo, G ;
Rosenberg, L ;
Prentki, M .
ENDOCRINOLOGY, 2003, 144 (09) :4154-4163
[29]   Glucose-regulated anaplerosis and cataplerosis in pancreatic β-cells -: Possible implication of a pyruvate/citrate shuttle in insulin secretion [J].
Farfari, S ;
Schulz, V ;
Corkey, B ;
Prentki, M .
DIABETES, 2000, 49 (05) :718-726
[30]   High glucose causes apoptosis in cultured human pancreatic Islets of Langerhans - A potential role for regulation of specific Bcl family genes toward an apoptotic cell death program [J].
Federici, M ;
Hribal, M ;
Perego, L ;
Ranalli, M ;
Caradonna, Z ;
Perego, C ;
Usellini, L ;
Nano, R ;
Bonini, P ;
Bertuzzi, F ;
Marlier, LNJL ;
Davalli, AM ;
Carandente, O ;
Pontiroli, AE ;
Melino, G ;
Marchetti, P ;
Lauro, R ;
Sesti, G ;
Folli, F .
DIABETES, 2001, 50 (06) :1290-1301