Identification and analysis of target factors for amelioration of pancreatic beta-cell function under diabetic conditions
| Project/Area Number |
18K16231
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Osaka University |
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Principal Investigator |
Shimo Naoki 大阪大学, 医学部附属病院, 医員 (10814064)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 膵β細胞 / 高血糖毒性 / 2型糖尿病 / インスリン分泌顆粒 / 酸化ストレス / 糖尿病 |
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| Outline of Final Research Achievements |
We frequently experience the gradual deterioration of blood glucose control in patients with type 2 diabetes, and glucose toxicity, which represents the dysfunction of pancreatic β-cells caused by chronic hyperglycemia, is involved in the pathophysiology. We hypothesized that glucose toxicity-sensitive genes, whose expressions were readily influenced by chronic hyperglycemia, played important roles in β-cell functions, and identified two novel factors, Tmem163 and Cox6a2. Our data suggest these factors contribute to β-cell functions through the maturation of insulin secretory granules and oxidative stress, respectively.
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| Academic Significance and Societal Importance of the Research Achievements |
2型糖尿病患者は増加の一途をたどるが、疾患の経過において認められる、膵β細胞機能低下およびそれに伴う血糖管理増悪をもたらす「高血糖毒性」のメカニズムは、これまで明らかにされていない。本研究により新規同定されたTmem163およびCox6a2は、膵β細胞が正常に機能する上で重要な役割を果たすことが示唆されており、特に2型糖尿病発症の初期段階に関わることが想定されている。膵β細胞機能低下を防ぐためには糖尿病初期からの治療が重要であることから、上記因子に関する解析は、新たな糖尿病治療法の開発に資することが期待される。
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Report
(4 results)
Research Products
(8 results)
