β-cell-specific inactivation of the mouse Ipf1/Pdx1 gene results in loss of the β-cell phenotype and maturity onset diabetes

被引：809

作者：

Ahlgren, U ^{[1
]}

Jonsson, J ^{[1
]}

Jonsson, L ^{[1
]}

Simu, K ^{[1
]}

Edlund, H ^{[1
]}

机构：

[1] Umea Univ, Dept Microbiol, S-90187 Umea, Sweden

来源：

GENES & DEVELOPMENT | 1998年 / 12卷 / 12期

关键词：

Ipf1/Pdx1; beta-cell-specific mutants; hormone production; glucose-sensing; diabetes;

D O I：

10.1101/gad.12.12.1763

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

To study the late beta-cell-specific function of the homeodomain protein IPF1/PDX1 we have generated mice in which the Ipf1/Pdx1 gene has been disrupted specifically in beta cells. These mice develop diabetes with age, and we show that IPF1/PDX1 is required for maintaining the beta cell identity by positively regulating insulin and islet amyloid polypeptide expression and by repressing glucagon expression. We also provide evidence that IPF1/PDX1 regulates the expression of Glut2 in a dosage-dependent manner suggesting that lowered IPF1/ PDX1 activity may contribute to the development of type II diabetes by causing impaired expression of both Glut2 and insulin.

引用

页码：1763 / 1768

页数：6

共 37 条

[1]

Ahlgren U, 1996, DEVELOPMENT, V122, P1409

[2] Independent requirement for ISL1 in formation of pancreatic mesenchyme and islet cells [J].