| Project/Area Number |
21591160
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
|
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| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
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| Co-Investigator(Kenkyū-buntansha) |
NOGUCHI Tohru 金沢大学, 医学系・研究科, 助教 (40456421)
|
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| Co-Investigator(Renkei-kenkyūsha) |
IKEWAKI Katsunori 防衛医科大学校, 老年内科, 教授 (40287199)
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 脂質代謝異常 / 家族性高コレステロール血症 / 安定同位体 / 常染色体劣性高コレステロール血症 / PCSK9 |
|---|
| Research Abstract |
The fractional catabolic rate(FCR) of low-density lipoprotein(LDL) apolipoprotein B(apoB) in a patient with autosomal recessive hypercholesterolemia(ARH) was 75% smaller, whereas direct removal of very-LDL apoB was dramatically greater compared with those of normal control subjects. Statin therapy normalized FCR of LDL apoB and increased direct removal of very-LDL in ARH patient. On the other hand, the FCR of patients with homozygous proprotein convertase subtilisin/kexin 9(PCSK9) gene mutation was 52% smaller than that of normal control subjects and normalized by statin therapy. Whereas, both production rate and direct removal of very-LDL was increased compared with those of normal control subjects, which were not changed by statin therapy.
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