Elucidation of an Asian type II diabetes mellitus using leptin receptor-deficient medaka
| Project/Area Number |
15K18389
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory animal science
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| Research Institution | Kyorin University (2016-2018)
National Institute for Basic Biology (2015) |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | メダカ / ヒト疾患モデル / 糖尿病網膜症 / 糖尿病性腎症 / 糖尿病 / 疾患モデル |
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| Outline of Final Research Achievements |
Our research using leptin receptor-deficient medaka would contribute to understanding the cause of Asian type 2 diabetes without obesity. The adult mutant did not become obesity and but showed signs of diabetes, such as fasting hyperglycemia and impaired insulin secretion, which was a late-onset disorder caused by excessive feeding at the post-juvenile stage. The mutant also showed histopathological characteristics similar to those in ocular and renal lesions of human and rodent models of diabetic retinopathy and nephropathy. Leptin receptor-deficient medaka would be an animal model for understanding type 2 diabetes without obesity and ocular/renal pathogenetic mechanisms.
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| Academic Significance and Societal Importance of the Research Achievements |
肥満は糖尿病のリスクである。しかし、本研究では、肥満になる時期にも注目する必要があることを明らかにしたことに社会的意義がある。メダカもヒトと同じような血糖値制御機構をもち、若年期に食べ過ぎるとその後成魚期に糖尿病になるが、若年期に食べ過ぎず、成魚期に初めて食べ過ぎる期間を設けた場合、そのメダカは糖尿病にならない。また、本研究の糖尿病メダカは、既存のモデル生物より早く網膜症等を示す、実験を遂行する上で有益なモデルであり、さらに外科的手術や薬剤処理をせずに、摂餌量の制御だけで腎症等を示す、ヒトへの外挿性を考慮するうえで有益なモデルであることを明らかにしたことに学術的意義がある。
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Report
(5 results)
Research Products
(14 results)
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[Journal Article] Abnormal nuclear morphology is independent of longevity in a zmpste24-deficient fish model of Hutchinson-Gilford progeria syndrome (HGPS)2018
Author(s)
Tonoyama Y, Shinya M, Toyoda A, Kitano T, Oga A, Nishimaki T, Katsumura T, Oota H, Wan MT, Yip BWP, Helen MOL, Chisada S, Deguchi T, Au DWT, Naruse K, Kamei Y, Taniguchi Y
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Journal Title
Comp Biochem Physiol C Toxicol Pharmacol
Volume: 209
Pages: 54-62
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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