| Project/Area Number |
15K15356
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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 |
Endocrinology
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | グルカゴン / アミノ酸 / ノックアウトマウス / 糖尿病 / 神経内分泌腫瘍 / ランゲルハンス島 / α細胞 / 細胞増殖制御 / グルカゴノーマ / 液性因子 / mTOR |
|---|
| Outline of Final Research Achievements |
Homozygous glucagon-GFP knock-in mice, which is deficient in all the peptide derived from proglucagon, are nomoglycemic and develop hyperplasia of GFP-positive islet alpha-like cells. To elucidate the regulatory mechanisms of alpha cell proliferation, subrenal capsule transplantation experiments were performed, and the result indicated that proliferation of alpha cells is regulated by a humoral factor(s) derived from liver. Although exploration to identify a specific humoral factor failed to identify such factors encoded by a specific gene, accumulating data suggested that hyperaminoacidemia under glucagon deficiency should be involved in accelerated proliferation of islet alpha cells.
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