| Project/Area Number |
23659143
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Hyogo University of Health Sciences |
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Principal Investigator |
BABA Akemichi 兵庫医療大学, 薬学部, 教授 (70107100)
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| Co-Investigator(Kenkyū-buntansha) |
SHINTANI Norihito 大阪大学, 薬学研究科, 准教授 (10335367)
HAYATA Atsuko 大阪大学, 連合小児発達学研究科, 助教 (70390812)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | シグナル情報伝達系 / ミトコンドリア / 2 型糖尿病 / 酸化ストレス / 膵β細胞 / 2型糖尿病 / 心臓 / 遺伝子改変マウス / 膵臓 / 糖尿病 / マイトファジー / ミトコンドリア病 |
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| Research Abstract |
This study performed functional analyses on a novel gene named hyperplasia-associated gene of pancreatic β-cell (HPGB). We confirmed that HPGB functions as an endogenous mitochondrial fusion inhibitor etc., found its possible roles in the regulation of oxidative stress and mitophagy, and identified amino acids involved in its fusion inhibition activity. In addition, we generated transgenic mice overexpressing HPGB in the pancreatic β-cell or cardiac muscle. Phenotypic analyses of the β-cell transgenic mice suggested that HPGB enhances β-cell proliferation and suppresses oxidative lipids accumulation in β-cells under the type 2 diabetic condition. Taken together, this study firstly revealed the physiopathological significance of HPGB.
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