Isolation of common causative gene for type 1 and 2 diabetes using diabetic NSY mouse.
| Project/Area Number |
15H04499
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Food science
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| Research Institution | Nagoya University |
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Principal Investigator |
Horio Fumihiko 名古屋大学, 生命農学研究科, 教授 (20165591)
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| Co-Investigator(Kenkyū-buntansha) |
大野 民生 名古屋大学, 医学系研究科, 准教授 (90293620)
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| Research Collaborator |
Kobayashi Misato
Murai Atsushi
Ikegami Hiroshi
Mori Hitoshi
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2017: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2016: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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| Keywords | 1型糖尿病 / 2型糖尿病 / 疾患感受性遺伝子 / 膵臓ランゲルハンス氏島 / インスリン分泌 / １型糖尿病 / ２型糖尿病 |
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| Outline of Final Research Achievements |
As NSY mice develop the phenotype of both type 1 diabetes (T1DM) and type 2 diabetes (T2DM), we tried to isolate a common causative gene for both T1DM and T2DM on chromosome 11. By using congenic strains possessing a partial part of NSY’s chromosome 11, we isolated three independent chromosomal regions for impaired insulin secretion (0-25.96 Mb), insulin resistance (44.45-48.49 Mb) and streptozotocin-inducible T1DM (48.49-71.70 Mb) on chromosome 11. Moreover, we selected candidate genes in each region. As a result, we could not isolate a common causative gene for both T1DM and T2DM, but this result contributes to identify a novel diabetogenic gene on mouse chromosome 11.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、NSYマウスの第11番染色体のT2DM遺伝子としてインスリン分泌不全を規定するものがセントロメア～25.96 Mb領域に、インスリン抵抗性を規定するものが48.49～71.70 Mb領域に、T1DM責任遺伝子が44.45～48.49 Mb領域に存在することを初めて明らかにした。主目的のT1DMとT2DMに共通した膵ラ氏島β細胞の遺伝子の同定については、インスリン分泌不全とT1DM感受性遺伝子の存在領域が分離したことから、目的に合致した遺伝子の発見には繋がらなかった。しかし、NSYマウスの第11番染色体上の3つの異なるタイプの糖尿病責任遺伝子の遺伝学的解剖と存在の証明に成功した。
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Report
(4 results)
Research Products
(7 results)
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[Journal Article] Genetic dissection of the fatty liver QTL Fl1sa by using congenic mice and identification of candidate genes in the liver and epididymal fat.2016
Author(s)
Suzuki, M., Kobayashi, M., Ohno, T., Kanamori, S., Tateishi, S., Murai, A. and Horio, F.
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Journal Title
BMC Genet.
Volume: 17
Issue: 1
Pages: 145-145
DOI
Related Report
Peer Reviewed / Open Access
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