Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes

被引：44

作者：

Butler, A. E. ^{[1
]}

Robertson, R. P. ^{[2
,3
,4
]}

Hernandez, R. ^{[1
]}

Matveyenko, A. V. ^{[1
]}

Gurlo, T. ^{[1
]}

Butler, P. C. ^{[1
]}

机构：

[1] Univ Calif Los Angeles, David Geffen Sch Med, Larry Hillblom Islet Res Ctr, Los Angeles, CA 90095 USA

[2] Univ Washington, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA 98195 USA

[3] Univ Washington, Dept Pharmacol, Div Metab Endocrinol & Nutr, Seattle, WA 98195 USA

[4] Univ Washington, Pacific NW Diabet Res Inst, Seattle, WA 98195 USA

来源：

DIABETOLOGIA | 2012年 / 55卷 / 11期

基金：

美国国家卫生研究院;

关键词：

Beta cell; Glucotoxicity; MafA; INSULIN-SECRETION; OXIDATIVE STRESS; GENE-EXPRESSION; MECHANISM;

D O I：

10.1007/s00125-012-2666-2

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The beta cell transcriptional factor musculoaponeurotic fibrosarcoma oncogene family A (MafA) regulates genes important for beta cell function. Loss of nuclear MafA has been implicated in beta cell dysfunction in animal models of type 2 diabetes. We sought to establish if nuclear MafA is less abundant in beta cell nuclei in humans with type 2 diabetes. Pancreas obtained at surgery from five non-diabetic individuals and six individuals with type 2 diabetes was immunostained for insulin, glucagon and MafA. Beta cell nuclear MafA was markedly decreased in type 2 diabetes (1.6 +/- 1.2% vs 46.3 +/- 8.3%, p < 0.001). Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.

引用

页码：2985 / 2988

页数：4

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