2005 Fiscal Year Final Research Report Summary
MafA differentiates rat intestinal cells into insulin-producing cells.
| Project/Area Number |
16590143
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
NAKAMURA Takaaki Shiga University of Medical Science, Medicine, Assistant Professor, 医学部, 助手 (30314157)
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| Co-Investigator(Kenkyū-buntansha) |
KASHIWAGI Atsunori Shiga University of Medical Science, Medicine, Professor, 医学部, 教授 (20127210)
KUDO Motoi Shiga University of Medical Science, Medicine, Professor, 医学部, 教授 (80108141)
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| Project Period (FY) |
2004 – 2005
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| Keywords | transcription factor / Mafa / rat intestine / diabetes mellitus / Pdx1 / insulin / gene therapy |
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| Research Abstract |
Recent studies have suggested that basic leucine zipper transcription factor MafA has a crucial role in pancreatic □-cell-specific insulin gene transcription. Thus, we investigated whether MafA overexpression in the intestine induces insulin production in small-intestinal epithelial cells in vivo. Recombinant adenovirus containing MafA gene(Ad-MafA) was prepared and administered orally to streptozocin-treated diabetic rats. Insulin gene expression was observed in the intestine by RT-PCR analysis, and then insulin protein was detected by immunohistochemical analysis after Ad-MafA administration. Furthermore, MafA overexpression in the intestine increased plasma insulin levels and ameliorated hyperglycemia. These results indicate that MafA overexpression in the intestine induces intestinal epithelial cells newly to produce and release insulin.
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