| Project/Area Number |
16K10003
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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 |
Pediatrics
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| Research Institution | Kurume University |
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Principal Investigator |
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| Research Collaborator |
Koga Yasutoshi
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | ミトコンドリア病 / GDF15 / FGF21 / 交絡因子 / バイオマーカー |
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| Outline of Final Research Achievements |
Our study is to reveal the confounding factors in GDF15 and FGF21 as biomarkers for mitochondrial disorders. The samples were used in normal control MELAS, CPEO/KSS, Leigh syndrome, multiple sclerosis, optic neuritis, and limbic encephalitis. The candidates were age, MCH, BUN, and Cr. GDF15 was slightly correlated with FGF21 (0.56), MCH (-0.42), BUN (0.51), and Cr (0.45). Especially, BUN and Cr were significant factors without age. GDF15 was increased in demyelinating diseases including multiple sclerosis, and especially limbic encephalitis was influenced with demyelination. GDF15 and FGF21 were slightly correlation in optic neuritis. Caution was warranted that GDF15 and FGF21 showed high levels in demyelinating diseases.
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| Academic Significance and Societal Importance of the Research Achievements |
GDF15とFGF21の明かな交絡因子は見つけられなかったが、候補となるものを見つけることができた。多発性硬化症の ような脱髄疾患では、GDF15もFGF21もともに上昇傾向を示す。辺縁系脳炎では、一部が脱髄を起こすしその影響を受けていることが示唆される。この成果をもとに、基礎研究と共同して、GDF15、FGF21がどうして高値になるかを明らかにしなければならない。
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