Mitochondrial dysfunction and type 2 diabetes

被引：1556

作者：

Lowell, BB

Shulmanz, GI

机构：

[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA

[2] Yale Univ, Sch Med, Dept Internal Med, Howard Hughes Med Inst, New Haven, CT 06536 USA

[3] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06536 USA

来源：

SCIENCE | 2005年 / 307卷 / 5708期

关键词：

D O I：

10.1126/science.1104343

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimutated insulin secretion by pancreatic beta cells. Defects in the former are responsible for insulin resistance, and defects in the latter are responsible for progression to hyperglycemia. Emerging evidence supports the potentially unifying hypothesis that both of these prominent features of type 2 diabetes are caused by mitochondrial dysfunction.

引用

页码：384 / 387

页数：4

共 58 条

[1] TRIPOD (TRoglitazone in the Prevention of Diabetes): A randomized, placebo-controlled trial of troglitazone in women with prior gestational diabetes mellitus
Azen, SP
Peters, RK
Berkowitz, K
Kjos, S
Xiang, A
Buchanan, TA
[J]. CONTROLLED CLINICAL TRIALS, 1998, 19 (02): : 217 - 231
[2] Visualizing superoxide production in normal and diabetic rat islets of Langerhans
Bindokas, VP
Kuznetsov, A
Sreenan, S
Polonsky, KS
Roe, MW
Philipson, LH
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (11) : 9796 - 9801
[3] Free fatty acids in obesity and type 2 diabetes:: defining their role in the development of insulin resistance and β-cell dysfunction
Boden, G
Shulman, GI
[J]. EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 2002, 32 : 14 - 23
[4] Glucose induces and leptin decreases expression of uncoupling protein-2 mRNA in human islets
Brown, JEP
Thomas, S
Digby, JE
Dunmore, SJ
[J]. FEBS LETTERS, 2002, 513 (2-3) : 189 - 192
[5] β-cell deficit and increased β-cell apoptosis in humans with type 2 diabetes
Butler, AE
Janson, J
Bonner-Weir, S
Ritzel, R
Rizza, RA
Butler, PC
[J]. DIABETES, 2003, 52 (01) : 102 - 110
[6] Increased uncoupling protein-2 levels in β-cells are associated with impaired glucose-stimulated insulin secretion -: Mechanism of action
Chan, CB
De Leo, D
Joseph, JW
McQuaid, TS
Ha, XF
Xu, F
Tsushima, RG
Pennefathner, PS
Salapatek, AMF
Wheeler, MB
[J]. DIABETES, 2001, 50 (06) : 1302 - 1310
[7] PATHOGENESIS OF NIDDM - A BALANCED OVERVIEW
DEFRONZO, RA
BONADONNA, RC
FERRANNINI, E
[J]. DIABETES CARE, 1992, 15 (03) : 318 - 368
[8] Structural and functional abnormalities in the islets isolated from type 2 diabetic subjects
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
[J]. DIABETES, 2004, 53 (03) : 624 - 632
[9] Pancreatic β-cell growth and survival in the onset of type 2 diabetes:: a role for protein kinase B in the Akt?
Dickson, LM
Rhodes, CJ
[J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2004, 287 (02): : E192 - E198
[10] Effects of free fatty acids on glucose transport and IRS-1-associated phosphatidylinositol 3-kinase activity
Dresner, A
Laurent, D
Marcucci, M
Griffin, ME
Dufour, S
Cline, GW
Slezak, LA
Andersen, DK
Hundal, RS
Rothman, DL
Petersen, KF
Shulman, GI
[J]. JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (02) : 253 - 259

← 1 2 3 4 5 6 →