Physiological and pathophysiological roles of KCNQ1 as a susceptibility gene for type 2 diabetes mellitus
| Project/Area Number |
15K09377
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Takamoto Iseki 東京大学, 医学部附属病院, 助教 (60431871)
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| Research Collaborator |
KUBOTA Naoto
NAKAYA Keizo
KUMAGAI Katsuyoshi
KUBOTA Tetsuya
INOUE Mariko
SAKURAI Yoshitaka
IWAMOTO Masahiko
YOSHIDA Masashi
HARA Kazuo
UEKI Kohjiro
KADOWAKI Takashi
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 2型糖尿病 / 疾患感受性遺伝子 / KCNQ1 / インスリン分泌 / 膵β細胞 |
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| Outline of Final Research Achievements |
Common genetic variations of KCNQ1 are associated with type 2 diabetes. In this study, we investigated the physiological and pathophysiological roles of KCNQ1 in glucose homeostasis with several genetically engineered mice. We have identified novel genetically engineered mice with loss-of-function KCNQ1 caused by a single-nucleotide mutation, which showed no obvious glucose intolerance. By contrast, mice with gain -of-function KCNQ1 in in the pancreatic beta cells were associated with a reduction of insulin secretion, leading to impaired glucose tolerance. Thus, our findings suggest that functional up-regulation and/or over-expression of KCNQ1 in the pancreatic beta cells play a crucial role in glucose metabolism in vivo.
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Report
(4 results)
Research Products
(4 results)
