Diabetes -: A signal for β-cell failure

被引：9

作者：

Avruch, J ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Dept Med, Diabet Unit, Boston, MA 02114 USA

[2] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA

[3] Harvard Univ, Sch Med, Boston, MA 02114 USA

来源：

NATURE | 1998年 / 391卷 / 6670期

关键词：

D O I：

10.1038/35998

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：

A hallmark of human type 2 diabetes is hyperglycaemia — an excess of glucose in the bloodstream. Normally, the pancreatic β-cell compensate for this by secreting more insulin, but this fail-safe mechanism seems to malfunction in patients with the condition. Now, by generating mice that lack the insulin-receptor substrate-2 (IRS-2) gene, one group has shown that IRS-2 may be responsible for both increased insulin resistance and reduced insulin compenation. The knockout mice develop a syndrome that closely resembles human type 2 diabetes and, importantly, they have fewer β-cells than wild-type mice.

引用

页码：846 / 847

页数：2

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