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Diabetes 54:1009-1022, 2005
© 2005 by the American Diabetes Association, Inc.

PDX-1/VP16 Fusion Protein, Together With NeuroD or Ngn3, Markedly Induces Insulin Gene Transcription and Ameliorates Glucose Tolerance

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

Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Osaka, Japan

Diabetes is the most prevalent and serious metabolic disease, and the number of diabetic patients worldwide is increasing. The reduction of insulin biosynthesis in pancreatic ß-cells is closely associated with the onset and progression of diabetes, and thus it is important to search for ways to induce insulin-producing cells in non–ß-cells. In this study, we showed that a modified form of the pancreatic and duodenal homeobox factor 1 (PDX-1) carrying the VP16 transcriptional activation domain (PDX-1/VP16) markedly increases insulin biosynthesis and induces various pancreas-related factors in the liver, especially in the presence of NeuroD or neurogenin 3 (Ngn3). Furthermore, in streptozotocin-induced diabetic mice, PDX-1/VP16 overexpression, together with NeuroD or Ngn3, drastically ameliorated glucose tolerance. Thus PDX-1/VP16 expression, together with NeuroD or Ngn3, markedly induces insulin gene transcription and ameliorates glucose tolerance. This approach warrants further investigation and may have utility in the treatment of diabetes.

Address correspondence and reprint requests to Hideaki Kaneto, MD, PhD, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. E-mail: kaneto{at}medone.med.osaka-u.ac.jp


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Copyright © 2005 by the American Diabetes Association.