Development of a novel antidiabetic drug based on the targeting of GnT-IVa glycosyltransferase
| Project/Area Number |
23790363
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Kumamoto University (2013)
Osaka University (2011-2012) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KOREKANE Hiroaki 独立行政法人理化学研究所, 疾患糖鎖研究チーム, 研究員 (50421912)
NAKAJIMA Kazuki 独立行政法人理化学研究所, 神経膜機能研究チーム, 研究員 (10442998)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 糖鎖修飾 / グルコーストランスポーター / グルコースセンサー機能 / 膵臓β細胞 / 糖転移酵素発現調節 / 糖尿病 / 高脂肪食 |
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| Research Abstract |
We have focused on the physiological and functional regulation mechanism of a glycosyltransferase "GnT-IVa", modulating the glucose sensor function of pancreatic beta cells, for developing a novel antidiabetic drug. We have revealed that high fat-diet induces significant oxidative stress in pancreatic beta cells that can be a trigger to suppress GnT-IVa expression and diminishes glucose stimulated insulin secretion in the pathogenesis of type 2 diabetes. Besides, we engineered to express GnT-IVa in pancreatic beta cells in vivo, and then revealed that they are resistant to the high fat-diet induced diabetes that strongly suggest that GnT-IVa is an important target to develop antidiabetic drugs. We established cell-based assay system for exploring the drug compounds enhancing GnT-IVa expression from chemical libraries.
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Report
(4 results)
Research Products
(21 results)
