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
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共 125 条
[1]   Intra-uterine transmission of disease [J].
Aerts, L ;
Van Assche, FA .
PLACENTA, 2003, 24 (10) :905-911
[2]   Dissociated insulinotropic sensitivity to glucose and carbachol in high-fat diet-induced insulin resistance in C57BL/6J mice [J].
Ahren, B ;
Simonsson, E ;
Scheurink, AJW ;
Mulder, H ;
Myrsen, U ;
Sundler, F .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1997, 46 (01) :97-106
[3]   Autonomic regulation of islet hormone secretion -: Implications for health and disease [J].
Ahrén, B .
DIABETOLOGIA, 2000, 43 (04) :393-410
[4]   Differential effect of inbred mouse strain (C57BL/6, DBA/2, 129T2) on insulin secretory function in response to a high fat diet [J].
Andrikopoulos, S ;
Massa, CM ;
Aston-Mourney, K ;
Funkat, A ;
Fam, BC ;
Hull, RL ;
Kahn, SE ;
Proietto, J .
JOURNAL OF ENDOCRINOLOGY, 2005, 187 (01) :45-53
[5]   The redox regulation of intermediary metabolism by a superoxide-aconitase rheostat [J].
Armstrong, JS ;
Whiteman, M ;
Yang, HY ;
Jones, DP .
BIOESSAYS, 2004, 26 (08) :894-900
[6]   TYPE 2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS, HYPERTENSION AND HYPERLIPEMIA (SYNDROME-X) - RELATION TO REDUCED FETAL GROWTH [J].
BARKER, DJP ;
HALES, CN ;
FALL, CHD ;
OSMOND, C ;
PHIPPS, K ;
CLARK, PMS .
DIABETOLOGIA, 1993, 36 (01) :62-67
[7]   Biochemical mechanism of lipid-induced impairment of glucose-stimulated insulin secretion and reversal with a malate analogue [J].
Boucher, A ;
Lu, DH ;
Burgess, SC ;
Telemaque-Potts, S ;
Jensen, MV ;
Mulder, H ;
Wang, MY ;
Unger, RH ;
Sherry, AD ;
Newgard, CB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (26) :27263-27271
[8]   A radical explanation for glucose-induced β cell dysfunction [J].
Brownlee, M .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (12) :1788-1790
[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]   Increased fatty acid desaturation and enhanced expression of stearoyl coenzyme A desaturase protects pancreatic β-cells from lipoapoptosis [J].
Busch, AK ;
Gurisik, E ;
Cordery, DV ;
Sudlow, M ;
Denyer, GS ;
Laybutt, DR ;
Hughes, WE ;
Biden, TJ .
DIABETES, 2005, 54 (10) :2917-2924