Akt and PTEN: β-cell mass and pancreas plasticity

被引：80

作者：

Elghazi, Lynda ^{[1
]}

Bernal-Mizrachi, Ernesto ^{[1
]}

机构：

[1] Washington Univ, Dept Internal Med, Div Endocrinol Metab & Lipid Res, Sch Med, St Louis, MO 63110 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2009年 / 20卷 / 05期

关键词：

PROTEIN-KINASE-B; ENDOPLASMIC-RETICULUM STRESS; GLYCOGEN-SYNTHASE KINASE-3-BETA; TRANSCRIPTION FACTOR FOXO1; INSULIN-RESISTANCE; GLUCOSE-HOMEOSTASIS; DIABETES-MELLITUS; SIGNALING PATHWAY; INDUCED APOPTOSIS; GENE-EXPRESSION;

D O I：

10.1016/j.tem.2009.03.002

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The capacity of pancreatic beta-cells to adapt to insulin resistance is crucial for glucose homeostasis and is a factor in the development of type 2 diabetes. The insulin receptor substrate (insulin receptor 2/phosphoinositide 3-kinase [PI3K]) pathway plays a crucial part in regulating beta-cell mass and function. The serine-threonine kinase Akt, also known as protein kinase B, is one of the major downstream targets of the PI3K pathway and is negatively regulated by phosphatase and tensin homologue deleted on chromosome 10. This Akt signaling pathway has recently been implicated in cell-cycle progression and survival of pancreatic beta-cells. Understanding the mechanisms that link Akt to modulation of beta-cell mass, function and plasticity will positively affect treatment of human diabetes.

引用

页码：243 / 251

页数：9

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