The investigation of the molecular mechanisms in COMT-deficiency-induced health problems

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460403
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pathological medical chemistry
• Research Institution: Kanazawa Medical University
• Principal Investigator: KANASAKI Keizo 金沢医科大学, 医学部, 准教授 (60589919)
• Project Period (FY): 2014-04-01 – 2017-03-31
• 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

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.

Free Research Field

メタボリックシンドローム、妊娠高血圧腎症