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A more recent version of this article appeared on April 15, 2005
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Papers In Press, published online ahead of print January 20, 2005
J. Biol. Chem, 10.1074/jbc.M412013200
Submitted on October 22, 2004
Revised on January 4, 2005
Accepted on January 20, 2005

A crucial role of MafA as a novel therapeutic target for diabetes

Hideaki Kaneto, Taka-aki Matsuoka, Yoshihisa Nakatani, Takeshi Miyatsuka, Munehide Matsuhisa, Masatsugu Hori, and Yoshimitsu Yamasaki

Department of Internal Medicine and Therapeutics, Osaka University, Suita 565-0871

Corresponding Author: kaneto{at}medone.med.osaka-u.ac.jp

MafA, a recently isolated pancreatic beta -cell-specific transcription factor, is a potent activator of insulin gene transcription. In this study, we show that MafA overexpression, together with PDX-1 and NeuroD, markedly increases insulin gene expression in the liver. Consequently, substantial amounts of insulin protein were induced by such combination. Furthermore, in streptozotocin-induced diabetic mice, MafA overexpression in the liver, together with PDX-1 and NeuroD, dramatically ameliorated glucose tolerance, while combination of PDX-1 and NeuroD was much less effective. These results suggest a crucial role of MafA as a novel therapeutic target for diabetes.


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