Investigation for the physiological and pathological significance of the interaction between COMT deficiency and homocysteine
Project/Area Number |
23790381
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Pathological medical chemistry
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Research Institution | Kanazawa Medical University |
Principal Investigator |
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Project Period (FY) |
2011 – 2013
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 妊娠高血圧腎症 / 糖尿病 / 脂肪肝 / メタボリックシンドロームボリックシンドローム / COMT / メタボリックシンドローム / 妊娠糖尿病 / インスリン / 2-methoxyestradiol / metabolic syndrome |
Research Abstract |
Life style related diseases such as diabetes, metabolic syndrome, and cancer, would be caused by the interaction between genetic factor, life style, and environmental factors. When considering the recent epidemic of such life style related diseases, suggesting that most of people are indeed sharing genetic background and therefore such background is probably acquired for the evolutional process of homo sapience. Applicant of this grant established first genetic mouse model of preeclampsia and revealed catechol metabolism defects in catechol-o-methyltransferase (COMT) deficiency in mice was one possible explanation of preeclampsia pathogenesis. Preeclampsia and metabolic defects in life style related diseases share symptoms, such as glucose intolerance, hypertension, and abnormal adiposity. In our current study using mouse models, we confirmed COMT is fragile and easy to be suppressed in the exposure of environmental factors, such as high fat diet fed and pregnancy.
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Report
(4 results)
Research Products
(97 results)
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[Journal Article] Eplerenone ameliorates the phenotypes of metabolic syndrome with NASH in liver-specific SREBP1c Tg mice fed high-fat and high-fructose diet2013
Author(s)
Wada T, Miyashita Y, Sasaki M, Aruga Y, Nakamura Y, Ishii Y, Sasahara M, Kanasaki K, Kitada M, Koya D, Shimano H, Tsuneki H, Sasaoka T
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Journal Title
Am J Physiol Endocrinol Metab
Volume: 305(11)
Related Report
Peer Reviewed
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[Journal Article] Reply to Regarding the mechanism of action of a proposed peptide agonist of the bone morphogenetic protein receptor activin-like kinase 32013
Author(s)
Sugimoto H, Lebleu VS, Bosukonda D, Keck P, Taduri G, Bechtel W, Okada H, Carlson W, Bey P, Rusckowski M, Tampe B, Tampe D, Kanasaki K, Zeisberg M, Kalluri R
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Journal Title
Nat Med
Volume: 19(7)
Pages: 810-811
Related Report
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[Journal Article] Eplerenone ameliorates the phenotypes of metabolic syndrome with NASH in liver-specific SREBP1c Tg mice fed high-fat and high-fructose diet2013
Author(s)
Wada T, Miyashita Y, Sasaki M, Aruga Y, Nakamura Y, Ishii Y, Sasahara M, Kanasaki K, Kitada M, Koya D, Shimano H, Tsuneki H, Sasaoka
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Journal Title
Am J Physiol Endocrinol Metab
Volume: 305
Issue: 11
Pages: E1415-E1425
DOI
Related Report
Peer Reviewed
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[Journal Article] Reply to Regarding the mechanism of action of a proposed peptide agonist of the bone morphogenetic protein receptor activin-like kinase 32013
Author(s)
Sugimoto H, Lebleu VS, Bosukonda D, Keck P, Taduri G, Bechtel W, Okada H, Carlson W, Bey P, Rusckowski M, Tampe B, Tampe D, Kanasaki K, Zeisberg M, Kalluri R
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Journal Title
Nature Medicine
Volume: 19
Issue: 7
Pages: 810-1
DOI
Related Report
Peer Reviewed
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[Journal Article] Activin-like kinase 3 is important for kidney regeneration and reversal of fibrosis2012
Author(s)
Sugimoto H, Lebleu VS, Bosukonda D, Keck P, Taduri G, Bechtel W, Okada H, Carlson W, Bey P, Rusckowski M, Tampe B, Tampe D, Kanasaki K, Zeisberg M, Kalluri R
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Journal Title
Nat Med
Volume: 18(3)
Pages: 396-404
Related Report
Peer Reviewed
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