| Project/Area Number |
26460403
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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 |
Pathological medical chemistry
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
金崎 めぐみ 金沢医科大学, 医学部, 助教 (50599355)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | COMT / メタボリックシンドローム / 妊娠高血圧腎症 / エストロゲン代謝 / アンジオテンシン / PPAR-g / 2-methoxyestradiol / metabolic syndrome / insulin / 生活習慣病 / 耐糖能異常 / 高血圧 |
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| Outline of Final Research Achievements |
This applicant reported the first genetic model of preeclampsia by showing that catechol-o-methytransferase (COMT) deficient mice, displaying defects in catechol metabolism, exhibited preeclampsia phenotype during gestation. Preeclamspia and metabolic syndrome share some of clinical manifestation, therefore this applicant hypothesized that COMT deficiency could be relevant for the pathogenesis of both preeclampsia and metabolic syndrome. Indeed some of genetic analysis in the past supported this applicant's hypothesis. By completion of this application, this applicant revealed that at least two major clinical symptom of metabolic syndrome, hypertension and glucose intolerance, could be explained by COMT deficiency. Therefore COMT deficiency could be relevant pathomechanism in both preeclampsia and metabolic syndrome.
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