Disruption of adiponectin causes insulin resistance and neointimal formation.

被引：1081

作者：

Kubota, N

Terauchi, Y

Yamauchi, T

Kubota, T

Moroi, M

Matsui, J

Eto, K

Yamashita, T

Kamon, J

Satoh, H

Yano, W

Froguel, P

Nagai, R

Kimura, S

Kadowaki, T ^{[1
]}

Noda, T

机构：

[1] Univ Tokyo, Grad Sch Med, Dept Metab Dis, Tokyo 1138655, Japan

[2] Tohoku Univ, Sch Med, Dept Mol Genet, Sendai, Miyagi 9808575, Japan

[3] Japanese Fdn Canc Res, Inst Canc, Dept Cell Biol, Tokyo 1708455, Japan

[4] Univ Tokyo, Grad Sch Med, Dept Cardiovasc Dis, Tokyo 1138655, Japan

[5] Lille Pasteur Inst, F-59000 Lille, France

[6] Lille Inst Biol, CNRS 8090, F-59000 Lille, France

[7] Toho Univ, Ohashi Hosp, Sch Med, Dept Internal Med 3, Tokyo 1530044, Japan

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2002年 / 277卷 / 29期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1074/jbc.C200251200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The adipocyte-derived hormone adiponectin has been proposed to play important roles in the regulation of energy homeostasis and insulin sensitivity, and it has been reported to exhibit putative antiatherogenic properties in vitro. In this study we generated adiponectin-deficient mice to directly investigate whether adiponectin has a physiological protective role against diabetes and atherosclerosis in vivo. Heterozygous adiponectin-deficient (adipo(+/-)) mice showed mild insulin resistance, while homozygous adiponectin-deficient (adipo(-/-)) mice showed moderate insulin resistance with glucose intolerance despite body weight gain similar to that of wild-type mice. Moreover, adipo(-/-) mice showed 2-fold more neointimal formation in response to external vascular cuff injury than wild-type mice (p = 0.01). This study provides the first direct evidence that adiponectin plays a protective role against insulin resistance and atherosclerosis in vivo.

引用

页码：25863 / 25866

页数：4

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