IRS2 takes center stage in the development of type 2 diabetes

被引：44

作者：

Brady, MJ ^{[1
]}

机构：

[1] Univ Chicago, Dept Med, Comm Mol Metab & Nutr, Chicago, IL 60637 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2004年 / 114卷 / 07期

关键词：

D O I：

10.1172/JC1200423108

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 etiology of type 2 diabetes is characterized by obesity, insulin and leptin resistance, and compensatory P cell hyperplasia followed by islet degeneration, resulting in the eventual dysregulation of glucose and lipid homeostasis. The recent identification of insulin receptor substrate 2 (IRS2) as a central player in the pathophysiology of many of these processes suggests a potentially unifying molecular link underlying the initiation and progression of type 2 diabetes (see the related articles beginning on pages 908 and 917).

引用

页码：886 / 888

页数：3

共 16 条

[1] ALTERNATIVE PATHWAY OF INSULIN SIGNALING IN MICE WITH TARGETED DISRUPTION OF THE IRS-1 GENE [J].

ARAKI, E ;

LIPES, MA ;

PATTI, ME ;

BRUNING, JC ;

HAAG, B ;

JOHNSON, RS ;

KAHN, CR .

NATURE, 1994, 372 (6502) :186-190

[2] Insulin and leptin as adiposity signals [J].

Benoit, SC ;

Clegg, DJ ;

Seeley, RJ ;

Woods, SC .

RECENT PROGRESS IN HORMONE RESEARCH, VOL 59: CARDIOVASCULAR ENDOCRINOLOGY & OBESITY, 2004, 59 :267-285

[3] Leptin signaling in the central nervous system and the periphery [J].

Bjorbæk, C ;

Kahn, BB .

RECENT PROGRESS IN HORMONE RESEARCH, VOL 59: CARDIOVASCULAR ENDOCRINOLOGY & OBESITY, 2004, 59 :305-331

[4] Pancreatic stem cells [J].

Bonner-Weir, S ;

Sharma, A .

JOURNAL OF PATHOLOGY, 2002, 197 (04) :519-526

[5] Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation [J].

Dor, Y ;

Brown, J ;

Martinez, OI ;

Melton, DA .

NATURE, 2004, 429 (6987) :41-46

[6] Insulin receptor substrate 2 plays a crucial role in β cells and the hypothalamus [J].

Kubota, N ;

Terauchi, Y ;

Tobe, K ;

Yano, W ;

Suzuki, R ;

Ueki, K ;

Takamoto, I ;

Satoh, H ;

Maki, T ;

Kubota, T ;

Moroi, M ;

Okada-Iwabu, M ;

Ezaki, O ;

Nagai, R ;

Ueta, Y ;

Kadowaki, T ;

Noda, T .

JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (07) :917-927

[7] Disruption of insulin receptor substrate 2 causes type 2 diabetes because of liver insulin resistance and lack of compensatory β-cell hyperplasia [J].

Kubota, N ;

Tobe, K ;

Terauchi, Y ;

Eto, K ;

Yamauchi, T ;

Suzuki, R ;

Tsubamoto, Y ;

Komeda, K ;

Nakano, I ;

Miki, H ;

Satoh, S ;

Sekihara, H ;

Sciacchitano, S ;

Lesniak, M ;

Aizawa, S ;

Nagai, R ;

Kimura, S ;

Akanuma, Y ;

Taylor, SI ;

Kadowaki, T .

DIABETES, 2000, 49 (11) :1880-1889

[8]

Lin XY, 2004, J CLIN INVEST, V114, P908, DOI 10.1172/JCI22217

[9] Mouse models of insulin resistance [J].

Nandi, A ;

Utamura, Y ;

Kahn, CR ;

Accili, D .

PHYSIOLOGICAL REVIEWS, 2004, 84 (02) :623-647

[10] New perspectives into the molecular pathogenesis and treatment of Type 2 diabetes [J].

Saltiel, AR .

CELL, 2001, 104 (04) :517-529

← 1 2 →