| Project/Area Number |
21591133
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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 |
Metabolomics
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| Research Institution | Osaka University |
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Principal Investigator |
|
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| Co-Investigator(Kenkyū-buntansha) |
KANETO Hideaki 大阪大学, 医学系研究科, 准教授 (80448034)
松久 宗英 徳島大学, 糖尿病臨床研究開発センター, 教授 (60362737)
|
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUHISA Munehide 徳島大学, 糖尿病臨床研究開発センター (60362737)
|
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
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| Keywords | 糖尿病 / Mafa / 膵β細胞 / 活性酸素 / C-Jun / MafA / c-Jun |
|---|
| Research Abstract |
The insulin gene transcription factor Mafa is known to regulate insulin biosynthesis and secretion, but there is no in vivo evidence of the patho-physiological involvement of Mafa in diabetes. To examine how Mafa is critical for glycemic control under diabetic conditions, we generated transgenic mice overexpressing Mafa conditionally and specifically in islet. cells of diabetic mice. The sustained expression of Mafa in diabetic mice resulted in significantly lower plasma glucose and higher plasma insulin levels. In these mice, Mafa restored the expression of insulin and other potential Mafa target genes including genes newly identified by microarray analysis, and improved. cell function. In addition, islet mass was significantly restored in these mice. These results demonstrate that restoration of Mafa expression in islet. cells preserves islet. cell function and mass, leading to the improvement of glycemic control in type 2 diabetes.
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